Key Points
Why This Research Matters
The Scalp Hair Follicle: A Distinct and Complex Organ
How Do Microbes Get to Your Skin Cells and Immune System?
The Immune Conversation: How Microbes Influence the Skin and Hair Follicle Immunity
What Actually Lives on Your Scalp?
Microbiome Changes in Scalp Diseases
What This Means for Patients
What This Review Could Not Answer
Practical Take-Home Points
Frequently Asked Questions
Source Information

Key Points

The scalp hosts up to one billion microorganisms per square centimeter, forming a personal microbiome influenced by genetics, environment, and age.
Hair follicles are active immune organs with specialized compartments that harbor microbes and regulate immune responses.
Commensal bacteria protect against pathogens and support immune function, so harsh antimicrobial overuse may not be beneficial.
Biofilms in conditions like folliculitis decalvans resist antibiotics, explaining why some scalp infections relapse after treatment.
Early-life microbial exposure appears critical for immune tolerance to skin bacteria; disruption may cause later inflammatory responses.

Why This Research Matters

A single square centimeter of human skin, along with its hair follicles and oil glands, can be inhabited by up to one billion microorganisms, including bacteria, fungi, and viruses. These tiny residents form a complex community known as the skin microbiome.

Its composition varies significantly across different skin regions of the same person, depending on pH, temperature, moisture, and sebum (oil) content. A wide range of external factors shape who lives on your skin, including the way you were born (vaginal versus cesarean delivery), your living environment (sunlight exposure, air temperature, humidity), lifestyle habits, the cosmetics you use, and even your genetic predispositions. These factors result in highly individual microbiomes — no two scalps are exactly alike.

Hair follicles (HFs) — the tube-like structures from which hair grows — extend from the skin surface deep into the dermis or even subcutaneous tissue. Each follicle connects directly to a sebaceous gland, forming what researchers call the "pilosebaceous unit." This creates a unique, lipid-rich, water-repelling (hydrophobic) niche where specific microorganisms thrive.

The Scalp Hair Follicle: A Distinct and Complex Organ

Of the approximately five million hair follicles formed during embryonic development, 100,000–150,000 are located on the scalp, ensuring cyclic hair growth throughout life. Their openings significantly increase the skin's surface area and, more importantly for microbial colonization, form pockets along the infundibulum (the upper funnel-shaped part of the follicle) that extend into deeper scalp skin layers.

The infundibulum is typically filled with sebum, cellular debris, and a diverse range of microorganisms — from viruses and bacteria to yeasts, fungi, and even mites. Its lining (epithelium) features a rich network of antigen-presenting cells (immune cells that "show" foreign substances to other immune cells) and active immune cell trafficking, making it a site of intensive communication with the external environment.

It is important to note that not all hair follicles are the same. Large terminal hair follicles (the thick, pigmented hairs on your scalp) have anagen bulbs (the growing base) that extend deep into subcutaneous tissue, while vellus hairs (the fine, thin hairs) are much smaller. The size of the sebaceous gland and its activity also differ across body regions. These differences substantially affect the reservoir function and microbiome of each follicle.

Interestingly, the hair follicle has a split personality when it comes to immunity. The upper part (infundibulum) is densely populated with immune cells. In contrast, immune-privileged sites exist around the bulge (where stem cells reside) and the anagen bulb (the deep growing portion). At these sites, immune cells are significantly reduced, and gradients of immunosuppressive mediators have been identified. This immune privilege protects the hair follicle during its growth cycles.

A "collapse" of this immune privilege is a key element in chronic scalp diseases. Whether the bulb or the bulge privilege is disturbed determines whether the hair follicle survives — as in alopecia areata (AA), where hair loss is reversible — or is permanently destroyed, as in cicatricial (scarring) alopecia.

How Do Microbes Get to Your Skin Cells and Immune System?

To understand how microbes interact with the body, researchers must consider where, how, and to what extent microbial material reaches living cells. Bacteria are generally in the low micrometer range in size, meaning penetration is largely restricted to the deeper infundibulum and sebaceous gland. While the upper compartments of the infundibulum are covered with a thick protective stratum corneum (the outermost skin layer), the deeper infundibulum is considered an area of higher permeability.

Bacteria can also form biofilms — organized communities encased in a protective matrix. For instance, Staphylococcus epidermidis (S. epidermidis) forms biofilms between the squamous cells of the outer three to ten layers of the stratified epithelium of normal dry skin. Cutibacterium acnes (C. acnes, formerly known as Propionibacterium acnes) penetrates deep into the sebaceous follicle, attaching to the hair shaft — more often in acne patients than in healthy controls. Biofilms shield bacteria from immune cells and from the skin's normal shedding process.

Unlike engineered particles, some bacteria carry enzymes that actively promote tissue penetration and invasion. Dermatophytes (fungi that cause ringworm), for example, invade deeply along the root sheaths (ectothrix pattern) and even into the hair shaft itself (endothrix pattern) in tinea capitis (scalp ringworm).

Larger studies on micro- and nanoparticle penetration show that microparticles largely remain on the skin surface but can reach the deeper infundibulum of scalp hair follicles. Even nanoparticles penetrate only at very limited rates, depending on their physical and chemical properties. However, mild disruption of the skin barrier can allow particles to move into living tissue, be taken up by cells, and trigger immune reactions.

Despite the skin barrier being robust enough to limit penetration of large molecules and particles to single events, such interactions occur regularly — most prominently in niches and pockets such as hair follicles and skin furrows. Researchers have hypothesized that the dense population of antigen-presenting cells around the infundibula reflects the central role these structures play in immune surveillance. Insights from transcutaneous vaccination studies suggest that mild inflammatory stimuli that activate antigen-presenting cells increase their uptake of large molecules across the skin barrier.

The Immune Conversation: How Microbes Influence the Skin and Hair Follicle Immunity

Numerous immune cells are stationed in the skin and around its appendages, in close proximity to microbiota. Langerhans cells (LCs) — predominantly concentrated in the epidermis and the outer root sheath (ORS) of the upper hair follicle — can extend their dendrites (branch-like projections) between keratinocytes (skin cells) to capture microbial antigens.

These cells interact with skin-resident memory T cells, which "remember" previously encountered antigens. Under normal conditions, LCs promote the activation and proliferation of regulatory T cells (Tregs) involved in maintaining immune tolerance. In the presence of a pathogen, however, they also stimulate pathogen-specific effector memory T cells.

Other immune players include skin-resident CD103+ dendritic cells, which sense changes in microbial communities. In the absence of inflammation, these cells stimulate the influx of IL-17A+CD8+ T cells into the epidermis — with the strongest stimulation observed in mice colonized with S. epidermidis. The presence of different commensal (harmless resident) species is associated with distinct differences in the released cytokine profile, meaning the composition of microbial communities can influence the skin's immune status.

Why Commensal Bacteria Matter

Commensals (the "good" bacteria that live on your skin) are considered essential for maintaining skin homeostasis. They protect the skin from colonization by pathogens, stimulate the production of complement system proteins and cytokines involved in immune responses, help decrease the magnitude of inflammation, and promote tissue repair.

Gene expression analysis comparing mice raised with microbiota versus germ-free mice showed upregulation of innate immune response genes (including Toll-like receptors [TLRs] and antimicrobial peptides [AMPs]) and genes involved in cytokine activity (such as cutaneous IL-1 signaling) in mice with normal flora. Additionally, the expression of genes involved in keratinocyte differentiation and cornification (hardening) was influenced by microbes.

Antimicrobial Peptides: Your Skin's Own Antibiotics

Keratinocytes — including follicular keratinocytes and sebocytes (oil gland cells) — protect the host while also shaping the microbiome by producing antimicrobial peptides (AMPs) with broad-spectrum activity against bacteria, fungi, viruses, and parasites. Some AMPs are always present, while others are produced in response to skin microbiota such as Cutibacterium.

Pattern recognition receptors on keratinocytes, such as TLRs, recognize pathogen-associated molecular patterns like lipopolysaccharide (LPS) from Gram-negative bacteria. Depending on the context, activating these receptors either initiates an immune response — releasing AMPs, cytokines, and chemokines — or inhibits inflammation.

Different AMPs have been found in distinct parts of the scalp hair follicle:

Human β-defensin 1 and 2: Found in all suprabasal layers of the epidermis, the distal and central parts of the outer root sheath (including the bulge), and the sebaceous gland. Weaker expression appears in the proximal ORS and inner root sheath (IRS).
Psoriasin: Present in the epidermis and distal outer root sheath of human scalp hair follicles.
RNase7: Expressed throughout the entire outer root sheath.
Bactericidal/permeability-increasing protein: Identified in the inner root sheath.

Both psoriasin and RNase7 are also found in the sebaceous gland and can be induced by specific microbial products. In scalp hair follicles, stimulating TLR4 with LPS triggers release of both RNase7 and psoriasin, whereas stimulating TLR5 with flagellin (a component of Gram-negative bacteria) produces only RNase7.

The strongest expression of AMPs is in the upper part of the hair follicle — precisely where the largest concentration of microbiota resides. These peptides likely prevent microorganisms, especially pathogens, from penetrating deeper into the follicle and help modulate the composition of the follicular microbiome.

Microbes That Fight Other Microbes

Microbes can also produce their own antimicrobial substances. S. epidermidis and S. hominis release lantibiotics that inhibit colonization by S. aureus (a common pathogen). A serine protease called glutamyl endopeptidase (Esp), produced by some S. epidermidis strains, can dissolve proteins essential for S. aureus biofilm formation.

However, commensals can sometimes do the opposite. Depending on dose, growth phase, and pH, some Cutibacterium species can induce aggregation (clumping) of S. aureus, potentially contributing to pathogen colonization.

The Critical Window in Early Life

Both hair follicle morphogenesis (development) and skin colonization with microbes during the neonatal period are crucial for the migration of regulatory T cells (Tregs) into hair follicles — and therefore for developing immune tolerance to skin commensals. This special subset of CD4+ T cells suppresses autoimmune responses and maintains immune balance in peripheral tissues.

In a neonatal mouse model and human skin explants, Scharschmidt and colleagues showed that the presence of skin microbes stimulates the expression of the chemokine Ccl20 within the infundibulum of developing hair follicles. The receptor for Ccl20 (Ccr6) was found on Tregs in neonatal skin and the thymus. This Ccl20-Ccr6 pathway drives the inflow of thymus-derived Tregs into hair follicles. Disrupting this process — either by temporarily blocking Treg migration or by delaying skin colonization with commensals until adulthood — resulted in skin inflammation and failure to establish tolerance to resident bacteria.

If establishing tolerance also occurs within a limited time window in humans, disruption of this process might result in inflammatory responses to antigens encountered later in life.

Tregs and Hair Growth

Beyond tolerance, Tregs appear to directly regulate the hair cycle. A recent study by Ali and colleagues found that Tregs accumulate near the bulge of telogen (resting) hair follicles and stimulate the proliferation and differentiation of stem cells, driving the transition to anagen (growth phase). Lack of these T cells impaired the follicle's ability to enter the growth phase — both after hair removal and during the natural hair cycle.

Whether microbes influence Treg activity in the skin after the neonatal period — and whether they thereby contribute to hair cycle regulation — remains an open question.

What Actually Lives on Your Scalp?

The scalp is rich in sebaceous glands, which produce sebum released through ducts into the infundibula and onto the skin surface. Although sebum has antimicrobial properties, some microbes thrive in this oily environment. Cutibacterium hydrolyzes triglycerides and releases free fatty acids that promote its own adherence. Malassezia and Corynebacterium species do not produce their own lipids and benefit directly from the lipids in sebum. Very little is known about the environmental conditions in the deeper follicle below the infundibulum, including oxygen tension.

Bacteria on the Scalp Surface

Scalp swabs have been the most common method for analyzing scalp microbiomes. In healthy individuals, the most abundant bacteria are:

Cutibacterium species (mostly C. acnes)
Staphylococcus species (mostly S. epidermidis)

Together, these two groups comprise approximately 90% of total gene sequences found in scalp swabs. Other, significantly less numerous species include Corynebacterium spp., Streptococcus spp., Acinetobacter spp., and Prevotella spp.

Some discrepancies exist between studies. For example, Perez-Perez and colleagues found a putatively lower representation of Cutibacterium species in scalp colonization. Shibagaki and colleagues studied age-related changes in the scalp bacteria of women and found that the older group (ages 60–76) had higher species richness and a marked increase in the number of minor species compared to the younger group (ages 21–37). These age-related shifts in scalp microbiome were correlated with changes in the oral bacterial flora.

Deeper Follicle Bacteria

Studies of microbes in deeper portions of scalp hair follicles are scarce. Gram-positive bacteria deep within the infundibulum have been detected in biopsy samples using light and electron microscopy. Matard and colleagues, using field emission scanning electron microscopy and confocal laser scanning microscopy on plucked hairs, captured structures compatible with bacterial biofilm located below the infundibular part and above the matrix zone in two of three healthy individuals. These biofilms comprised bacilli that morphologically corresponded to C. acnes.

Fungi on the Scalp (Mycobiome)

Most studies of scalp fungi rely on swab samples. Malassezia species largely dominate the scalp, with Malassezia globosa (M. globosa) and M. restricta being the most abundant species. Other fungi identified on healthy scalps include Ascomycota (Acremonium spp., Didymella bryoniae), other Basidiomycota (Cryptococcus liquefaciens and C. diffluens), Coniochaeta spp., and Rhodotorula spp.

Children under age 14 have a more diverse mycobiome, with a relatively lower proportion of Malassezia species compared to adults in their 20s–30s. This is most likely because sebaceous glands have lower activity and different sebum composition before puberty. Yeasts have also been identified in the infundibulum using light and electron microscopy on biopsy samples and in vivo with confocal laser scanning microscopy.

Mites and Viruses

The scalp is not only home to bacteria and fungi:

Demodex folliculorum is usually found in the follicular infundibulum
Demodex brevis is located in sebaceous glands
Dermatophagoides spp. and Euroglyphus spp. were identified by Naspitz and colleagues in material vacuumed from the scalp surface
Human papilloma virus (HPV) was detected in plucked hairs and in scales collected from the scalps of healthy volunteers

Microbiome Changes in Scalp Diseases

The strongest evidence linking scalp microorganisms to disease has been found in seborrheic dermatitis/dandruff and in a type of scarring hair loss called folliculitis decalvans (FD). Antimicrobial treatment brings transient success in most cases. However, frequent recurrences, lack of efficacy in some patients, and the additional need for anti-inflammatory therapy during acute flare-ups indicate the complexity of these conditions.

Seborrheic Dermatitis and Dandruff

Seborrheic dermatitis is an inflammatory skin condition that develops in sebum-rich areas. Dandruff is considered a mild type of seborrheic dermatitis limited to the scalp. For years, the condition has been associated with an inflammatory response to yeasts — specifically Malassezia species. The exact disease mechanism is not fully understood, but it involves an interplay between the yeasts, sebum, and the host's immune response.

Folliculitis Decalvans

Folliculitis decalvans is a form of scarring alopecia. Researchers have identified structures compatible with bacterial biofilm in plucked hair follicles from patients with FD, although similar structures were also found in healthy individuals. The biofilm hypothesis is supported by several observations:

The disease persists despite transiently effective antibiotic therapy
Histology shows infiltration of polymorphonuclear neutrophils (a type of white blood cell) that destroy the follicle but cannot destroy biofilms
Patients generally have a normal immune background

The current hypothesis is that an initially non-pathogenic biofilm may become more extensive and transform into a pathogenic form that causes inflammation. Antibiotic treatment may kill the planktonic (free-floating) form of bacteria released from biofilms and temporarily relieve symptoms, but the remaining biofilm cells form the nidus (source) of chronic infection.

Androgenetic Alopecia

Androgenetic alopecia (AGA), commonly known as male or female pattern hair loss, features shortening of the anagen (growth) phase and slowly progressive miniaturization of the hair follicle. While the microbiome's role in AGA is not yet as well studied as in dandruff or FD, the review suggests that microbial influence on inflammation and hair cycle regulation may be relevant to this condition as well.

What This Means for Patients

This research highlights that your scalp is a complex ecosystem, not just a surface to be cleaned. The health of your hair follicles depends on a delicate balance between the microorganisms that live there and your immune system's response to them.

For patients with chronic scalp conditions such as dandruff, seborrheic dermatitis, or folliculitis decalvans, this has practical implications:

Antibiotic and antifungal treatments can provide relief but may not cure the underlying condition, especially if biofilms are involved
Anti-inflammatory therapy is often needed in addition to antimicrobial treatment, particularly during acute flare-ups
The recurrence of symptoms after treatment is common and expected due to the complex interplay of microbes, sebum, and immunity

The finding that Tregs help drive hair follicle regeneration suggests that therapies supporting immune tolerance or modulating the microbiome could one day be developed to support hair growth. However, these are still early research findings.

What This Review Could Not Answer

The authors acknowledge several important knowledge gaps:

Most microbiome studies use scalp surface swabs, which do not reveal what is happening in the deeper parts of the hair follicle
Studies of the deeper follicle microbiome are scarce, and the level of organization and interaction within this compartment is poorly understood
Whether microbes influence the activity and maintenance of Tregs in the skin after the neonatal period — and whether they contribute to hair cycle regulation in adults — remains unknown
The exact mechanisms linking microbial shifts to diseases such as acne vulgaris and hidradenitis suppurativa remain to be determined
Very little is known about the environmental conditions (such as oxygen tension) below the infundibulum

Practical Take-Home Points

Your scalp microbiome is personal and complex. The mix of microbes on your scalp is influenced by your genetics, environment, age, and even how you were born.
Commensal bacteria are protective. They help prevent pathogen colonization, support immune function, and promote tissue repair — so harsh antimicrobial overuse may not always be beneficial.
Dandruff and seborrheic dermatitis involve yeast overgrowth. Treatments that target Malassezia yeasts are effective in the short term, but recurrences are common.
Biofilms may explain stubborn scalp infections. In conditions like folliculitis decalvans, bacteria can organize into biofilms that resist antibiotics — which is why some patients relapse after treatment. Combined antimicrobial and anti-inflammatory approaches are often needed.
The immune system of the hair follicle is delicate. Loss of immune privilege in hair follicles is a key event in autoimmune hair loss conditions such as alopecia areata and lichen planopilaris, which is why immunosuppressive treatments are used clinically.
Early-life microbial exposure matters. The neonatal period appears to be a critical window for developing immune tolerance to skin bacteria. Disruption of this process may lead to inflammatory skin responses later in life.

Frequently Asked Questions

What is the scalp microbiome and why does it matter for hair health?

The scalp microbiome is the community of up to one billion microorganisms per square centimeter living on your scalp and in hair follicles. These microbes interact with your immune system and can influence normal hair growth and chronic inflammatory scalp diseases, making the balance between them important for scalp health.

Can microbes on my scalp cause hair loss?

Yes, some scalp conditions linked to microbes can cause hair loss. For example, folliculitis decalvans is a scarring alopecia associated with bacterial biofilms. Seborrheic dermatitis and dandruff involve yeast overgrowth. Additionally, immune changes triggered by microbes may affect hair follicle regeneration, but more research is needed.

What is a biofilm and how does it affect scalp infections?

A biofilm is an organized community of bacteria encased in a protective matrix. In folliculitis decalvans, biofilms in hair follicles resist antibiotics, so treatment may kill free-floating bacteria but the biofilm remains, causing chronic infection and relapse. This explains why some scalp infections are stubborn and require combined antimicrobial and anti-inflammatory therapy.

Why do dandruff and seborrheic dermatitis keep coming back after treatment?

Dandruff and seborrheic dermatitis are associated with an inflammatory response to Malassezia yeasts in sebum-rich areas. Treatments targeting these yeasts work temporarily, but the condition recurs frequently because of the complex interplay between yeasts, sebum, and your immune system. Anti-inflammatory therapy is often needed during flare-ups, but the underlying balance is hard to restore permanently.

Are antibiotics always effective for scalp conditions caused by bacteria?

Antibiotics can provide temporary relief for bacterial scalp conditions like folliculitis decalvans, but they are not always a cure. Bacteria form biofilms that resist antibiotics, so symptoms often return. Some patients do not respond to antibiotics at all, and anti-inflammatory treatment is usually needed during acute flare-ups.

Is early-life microbial exposure linked to later scalp problems?

Research in mice and human skin suggests the neonatal period is a critical time for developing immune tolerance to skin bacteria. Disrupting this process can lead to skin inflammation and failure to tolerate resident bacteria. Whether this applies to humans and later scalp diseases is not yet fully known, but it is an area of active study.

Source Information

Original Article Title: microbiome in scalp hair follicle biology and disease Vogt Charite

DOI: 10.1111/exd.13935

Authors: Katarzyna Polak-Witka, Lidia Rudnicka, Ulrike Blume-Peytavi, Annika Vogt

Journal: Experimental Dermatology, 2020; Volume 29, pages 286–294

Published: Received October 1, 2018; Revised March 2, 2019; Accepted March 18, 2019