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The Extracellular Matrix in Skin Inflammation and Infection

Pfisterer, Karin, Shaw, Lisa E., Symmank, Dörte, Weninger, Wolfgang·2021·Frontiers in Cell and Developmental Biology
DOI 10.3389/fcell.2021.682414PMC PMC8290172
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Abstract

The extracellular matrix (ECM) is an integral component of all organs and plays a pivotal role in tissue homeostasis and repair. While the ECM was long thought to mostly have passive functions by providing physical stability to tissues, detailed characterization of its physical structure and biochemical properties have uncovered an unprecedented broad spectrum of functions. It is now clear that the ECM not only comprises the essential building block of tissues but also actively supports and maintains the dynamic interplay between tissue compartments as well as embedded resident and recruited inflammatory cells in response to pathologic stimuli. On the other hand, certain pathogens such as bacteria and viruses have evolved strategies that exploit ECM structures for infection of cells and tissues, and mutations in ECM proteins can give rise to a variety of genetic conditions. Here, we review the composition, structure and function of the ECM in cutaneous homeostasis, inflammatory skin diseases such as psoriasis and atopic dermatitis as well as infections as a paradigm for understanding its wider role in human health.

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FIGURE 1 Human skin. The outermost layer of human skin is built by stratified epidermis. The bottom layer is called stratum basale and contains proliferating basal keratinocytes that are anchored to the basement membrane. While differentiating, they migrate from the stratum basale, through the stratum spinosum, stratum granulosum, and the stratum lucidum (not shown) to the stratum corneum. The vascularized dermis can further be separated into the upper papillary and the lower reticular dermis. Skin appendages, such as hair follicles, are embedded in the dermis and reach through the epidermis, whereas other appendages reside mostly in the dermis. The innermost skin layer is called hypodermis and is built by fat storing adipocytes. Note that not all skin appendages, and skin cells are shown.
FIGURE 1 Human skin. The outermost layer of human skin is built by stratified epidermis. The bottom layer is called stratum basale and contains proliferating basal keratinocytes that are anchored to the basement membrane. While differentiating, they migrate from the stratum basale, through the stratum spinosum, stratum granulosum, and the stratum lucidum (not shown) to the stratum corneum. The vascularized dermis can further be separated into the upper papillary and the lower reticular dermis. Skin appendages, such as hair follicles, are embedded in the dermis and reach through the epidermis, whereas other appendages reside mostly in the dermis. The innermost skin layer is called hypodermis and is built by fat storing adipocytes. Note that not all skin appendages, and skin cells are shown.CC BY · PubMed Central
FIGURE 2 Structure of pro-collagen and assembled collagen. (A) Three left-handed α-helices (left) form a right-handed collagen superhelix (middle) within collagen-producing cells. Once secreted to the extracellular space, enzymes cleave off the N- and C-terminal parts to form fully functional collagen (right). (B) Different forms of collagen assemble into diverse structures. Fibrillar collagen molecules assemble into collagen fibrils that are stabilized by crosslinking (type I, III, V). The net-forming collagen type IV can build a meshwork that is highly flexible compared to rigid fibrils. Non-classical collagens, such as type V and FACIT interact with collagen fibrils to enhance stability. Beaded collagen (type VI) links collagen type IV to collagen type I and III and increases tissue elasticity. Collagen type VII assembles into fibrils that anchor the BM to the papillary dermis and maintain tissue integrity.
FIGURE 2 Structure of pro-collagen and assembled collagen. (A) Three left-handed α-helices (left) form a right-handed collagen superhelix (middle) within collagen-producing cells. Once secreted to the extracellular space, enzymes cleave off the N- and C-terminal parts to form fully functional collagen (right). (B) Different forms of collagen assemble into diverse structures. Fibrillar collagen molecules assemble into collagen fibrils that are stabilized by crosslinking (type I, III, V). The net-forming collagen type IV can build a meshwork that is highly flexible compared to rigid fibrils. Non-classical collagens, such as type V and FACIT interact with collagen fibrils to enhance stability. Beaded collagen (type VI) links collagen type IV to collagen type I and III and increases tissue elasticity. Collagen type VII assembles into fibrils that anchor the BM to the papillary dermis and maintain tissue integrity.CC BY · PubMed Central
FIGURE 3 ECM in healthy mammalian skin. (A) Skin is composed of the epidermis (top part), dermis (mid part) and adipose cell-rich hypodermis (lower part) and resembles a highly accessible model tissue to study epithelia, connective tissue and extracellular matrix (ECM) structures specific for those layers. The BM (purple) connects the epidermis to the dermis, which is comprised of interstitial matrix. (B) The dominant structural component in the BM is collagen type IV, which builds a meshwork with interspersed laminin and fibronectin. Together they build the basis for keratinocyte attachment via integrins. Collagen type VII reaches into the papillary dermis and stabilizes the dermal-epidermal junction. (C) In the dermis collagen type I and fibronectin build a fibrillary structure that allows cell adhesion and migration through the matrix. Shown is a fibroblast attaching to collagen and fibronectin via integrins.
FIGURE 3 ECM in healthy mammalian skin. (A) Skin is composed of the epidermis (top part), dermis (mid part) and adipose cell-rich hypodermis (lower part) and resembles a highly accessible model tissue to study epithelia, connective tissue and extracellular matrix (ECM) structures specific for those layers. The BM (purple) connects the epidermis to the dermis, which is comprised of interstitial matrix. (B) The dominant structural component in the BM is collagen type IV, which builds a meshwork with interspersed laminin and fibronectin. Together they build the basis for keratinocyte attachment via integrins. Collagen type VII reaches into the papillary dermis and stabilizes the dermal-epidermal junction. (C) In the dermis collagen type I and fibronectin build a fibrillary structure that allows cell adhesion and migration through the matrix. Shown is a fibroblast attaching to collagen and fibronectin via integrins.CC BY · PubMed Central
FIGURE 4 Different modes of cell migration in three-dimensional (3D) matrix. Cells can migrate through 3D matrix using different ways of motility, such as mesenchymal, amoeboid and lobopodial migration. (A) Mesenchymal migration is characterized by high adhesions and cell protrusions at the leading edge that align along collagen fibers. Cells that mainly use mesenchymal migration leave behind a tunnel in the ECM that can be utilized by following cells as tracks. (B) In contrast, amoeboid cell migration is less dependent on matrix adhesions. Cells show strong cell body and nucleus deformation during migration through tight spaces and generally choose the path of least resistance. (C) Lobopodial migration shows features of mesenchymal and amoeboid migration and typically has bleb protrusions at the migration front. Cells using one form of migration can change to using another form dependent on the environment.
FIGURE 4 Different modes of cell migration in three-dimensional (3D) matrix. Cells can migrate through 3D matrix using different ways of motility, such as mesenchymal, amoeboid and lobopodial migration. (A) Mesenchymal migration is characterized by high adhesions and cell protrusions at the leading edge that align along collagen fibers. Cells that mainly use mesenchymal migration leave behind a tunnel in the ECM that can be utilized by following cells as tracks. (B) In contrast, amoeboid cell migration is less dependent on matrix adhesions. Cells show strong cell body and nucleus deformation during migration through tight spaces and generally choose the path of least resistance. (C) Lobopodial migration shows features of mesenchymal and amoeboid migration and typically has bleb protrusions at the migration front. Cells using one form of migration can change to using another form dependent on the environment.CC BY · PubMed Central
FIGURE 5 ECM changes in skin inflammation. Inflammatory skin diseases can alter the composition and structure of the ECM. (A) In healthy skin collagen type IV builds a network with interspersed laminin to form the BM. This provides attachment points for basal keratinocytes of the epidermis and forms a protective layer to control leukocyte navigation through adjusted gap sizes and limits entry of harmful invaders via incorporation of sticky PG/GAGs. (B) Psoriasis is defined by high infiltration of IL-17 and IL-22 producing T helper cells. The BM in psoriasis is highly unstructured and thicker compared to healthy skin and shows elevated levels of laminin and fibronectin. (C) In atopic dermatitis, which is a T helper 2-driven inflammatory skin disease, collagen type IV and fibronectin are decreased, resulting in a thinner BM. Increased hyaluronan and MMPs are further characteristic for atopic dermatitis (not illustrated here). Not all relevant immune cells are illustrated.
FIGURE 5 ECM changes in skin inflammation. Inflammatory skin diseases can alter the composition and structure of the ECM. (A) In healthy skin collagen type IV builds a network with interspersed laminin to form the BM. This provides attachment points for basal keratinocytes of the epidermis and forms a protective layer to control leukocyte navigation through adjusted gap sizes and limits entry of harmful invaders via incorporation of sticky PG/GAGs. (B) Psoriasis is defined by high infiltration of IL-17 and IL-22 producing T helper cells. The BM in psoriasis is highly unstructured and thicker compared to healthy skin and shows elevated levels of laminin and fibronectin. (C) In atopic dermatitis, which is a T helper 2-driven inflammatory skin disease, collagen type IV and fibronectin are decreased, resulting in a thinner BM. Increased hyaluronan and MMPs are further characteristic for atopic dermatitis (not illustrated here). Not all relevant immune cells are illustrated.CC BY · PubMed Central
FIGURE 6 Filopodia grab virus particles off the matrix. Viruses that enter tissues stick to ECM proteins, such as HSPG, or freely diffuse in the interstitial fluid. Upon cell infection some viruses modify the cellular cytoskeleton and are able to induce cell protrusions called filopodia. When filopodia explore and interact with components of the ECM, they encounter freely floating or HSPG-bound virus particles and pick them off the matrix. Viruses hop from matrix HSPG onto secondary cell membrane HSPG and can surf along the filopodia shaft toward the cell body, where they invade and infect the target cell.
FIGURE 6 Filopodia grab virus particles off the matrix. Viruses that enter tissues stick to ECM proteins, such as HSPG, or freely diffuse in the interstitial fluid. Upon cell infection some viruses modify the cellular cytoskeleton and are able to induce cell protrusions called filopodia. When filopodia explore and interact with components of the ECM, they encounter freely floating or HSPG-bound virus particles and pick them off the matrix. Viruses hop from matrix HSPG onto secondary cell membrane HSPG and can surf along the filopodia shaft toward the cell body, where they invade and infect the target cell.CC BY · PubMed Central

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Metadata

Authors
Pfisterer, K., Shaw, L. E., Symmank, D., & Weninger, W.
Venue
Frontiers in Cell and Developmental Biology
Publisher
Frontiers Media SA
Published
2021-07-06
Volume
9
ISSN
2296-634X
DOI
10.3389/fcell.2021.682414
PMC
PMC8290172
Cited by
244
References
14
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • Vienna Science and Technology Fund
  • Amt der NÖ Landesregierung

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: The Extracellular Matrix in Skin Inflammation and Infection. https://app.cochat.ai/papers/10.3389/fcell.2021.682414
The paper
Pfisterer, K., Shaw, L. E., Symmank, D., & Weninger, W. (2021). The Extracellular Matrix in Skin Inflammation and Infection. Frontiers in Cell and Developmental Biology. https://doi.org/10.3389/fcell.2021.682414