Altered Skin and Gut Microbiome in Hidradenitis Suppurativa

McCarthy, S.; Barrett, Maurice P. J.; Kirthi, Shivashini; Pellanda, Paola; Vlčková, Klára; Tobin, Anne-Marie; Murphy, Michael; Shanahan, Fergus; O’Toole, Paul W.

doi:10.1016/j.jid.2021.05.036

Cited by 49 publications

(58 citation statements)

References 81 publications

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“…While HS is not a primary infectious disease, dysbiosis has been identified as one potential pathogenic pathway. 21 BTX directly decreases apocrine sweat production. This may decrease the tendency for follicular rupture and the spread of follicular material through the dermis, which exacerbates inflammation and formation of sinus tracts.…”

Section: Discussionmentioning

confidence: 97%

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Hyperhidrosis treatments in hidradenitis suppurativa: A systematic review

Shih

Lee

Seivright

et al. 2021

Dermatologic Therapy

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Hyperhidrosis impairs quality of life (QOL) in hidradenitis suppurativa (HS) patients and may exacerbate HS. However, there is limited literature on whether hyperhidrosis treatments improve HS disease. To systematically review literature on efficacy and tolerability of hyperhidrosis treatments in HS patients. In May 2021, MEDLINE and EMBASE databases were systematically searched by two reviewers per PRISMA guidelines for articles on hyperhidrosis and HS. Sixteen articles met inclusion criteria (2 randomized controlled trials [RCTs], one case-control study, three cross-sectional studies, 10 case-studies/ series), encompassing 252 HS patients across studies. They examined botulinum toxin A (BTX-A) (n = 6) and B (BTX-B) (n = 1), suction-curettage (n = 1), diode laser (n = 1), and microwave-based energy device (MED) (n = 3). Overall, BTX treatments improve HS severity, QOL, hyperhidrosis, and were well-tolerated. Suction-curettage did not improve disease. One HS patient tolerated diode laser well, with improvement in sweating and HS. One RCT studying MED was discontinued due to adverse events. Two studies reported MED-induced HS. BTX was overall helpful in HS patients, including in patients without concomitant hyperhidrosis. However, more prospective studies are needed to examine its utility in HS. There is potential harm of MEDs in HS. Most studies examining hyperhidrosis treatments in HS patients are low level of evidence. Larger RCTs should examine the efficacy and tolerability of hyperhidrosis treatments in HS.

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Section: Discussionmentioning

confidence: 97%

“…By reducing hyperhidrosis, BTX may be reducing moist environments for bacterial proliferation. While HS is not a primary infectious disease, dysbiosis has been identified as one potential pathogenic pathway 21 . BTX directly decreases apocrine sweat production.…”

Section: Discussionmentioning

confidence: 99%

Hyperhidrosis treatments in hidradenitis suppurativa: A systematic review

Shih

Lee

Seivright

et al. 2021

Dermatologic Therapy

View full text Add to dashboard Cite

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“…Total community DNA was extracted from fecal samples by a combined Repeat Bead Beating – Qiagen DNA extraction method, and the V3 dash V4 region of the 16S gene was amplified and sequenced as previously described. 52 The uniquely barcoded amplicons were sequenced on an Illumina MiSeq platform (Illumina, California, USA) utilizing 2 × 300 bp chemistry.…”

Section: Methodsmentioning

confidence: 99%

A high-risk gut microbiota configuration associates with fatal hyperinflammatory immune and metabolic responses to SARS-CoV-2

et al. 2022

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Protection against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and associated clinical sequelae requires well-coordinated metabolic and immune responses that limit viral spread and promote recovery of damaged systems. However, the role of the gut microbiota in regulating these responses has not been thoroughly investigated. In order to identify mechanisms underpinning microbiota interactions with host immune and metabolic systems that influence coronavirus disease 2019 (COVID-19) outcomes, we performed a multi-omics analysis on hospitalized COVID-19 patients and compared those with the most severe outcome (i.e. death, n = 41) to those with severe non-fatal disease (n = 89), or mild/moderate disease (n = 42), that recovered. A distinct subset of 8 cytokines (e.g. TSLP) and 140 metabolites (e.g. quinolinate) in sera identified those with a fatal outcome to infection. In addition, elevated levels of multiple pathobionts and lower levels of protective or anti-inflammatory microbes were observed in the fecal microbiome of those with the poorest clinical outcomes. Weighted gene correlation network analysis (WGCNA) identified modules that associated severity-associated cytokines with tryptophan metabolism, coagulation-linked fibrinopeptides, and bile acids with multiple pathobionts, such as Enterococcus . In contrast, less severe clinical outcomes are associated with clusters of anti-inflammatory microbes such as Bifidobacterium or Ruminococcus , short chain fatty acids (SCFAs) and IL-17A. Our study uncovered distinct mechanistic modules that link host and microbiome processes with fatal outcomes to SARS-CoV-2 infection. These features may be useful to identify at risk individuals, but also highlight a role for the microbiome in modifying hyperinflammatory responses to SARS-CoV-2 and other infectious agents.

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“…Compared to other skin loci, intertriginous areas affected in HS have a high density of pilosebaceous-apocrine units, higher temperature and moisture, but lower oxygen availability all contributing to specific microbiome composition and increased risk of dysbiosis ( 1 , 2 , 5 , 18 ). Systemic factors such as obesity, diabetes and nicotine use can also contribute to microbial dysbiosis and HS pathogenesis ( 1 , 19 , 20 ), and may correlate with the altered gut microbiome found in HS patients ( 21 , 22 ). Although it remains to be resolved if dysbiosis is a primary trigger or a consequence of HS, multiple studies provide insights into the microbiome composition at early and advanced stages of the disease.…”

Section: Microbial Dysbiosis In Hsmentioning

confidence: 99%

Innate immunity and microbial dysbiosis in hidradenitis suppurativa – vicious cycle of chronic inflammation

et al. 2022

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Hidradenitis Suppurativa (HS) is a chronic multifactorial inflammatory skin disease with incompletely understood mechanisms of disease pathology. HS is characterized by aberrant activation of the innate immune system, resulting in activation of pathways that aim to protect against pathogenic microorganisms, and also contribute to failure to resolve inflammation. Imbalance in innate immunity is evident in deregulation of host antimicrobial peptides (AMPs) and the complement system associated with the microbiome dysbiosis. The pathology is further complicated by ability of pathogens associated with HS to overcome host immune response. Potential roles of major AMPs, cathelicidin, defensins, dermcidin, S100 proteins, RNAse 7 and complement proteins are discussed. Dysregulated expression pattern of innate immunity components in conjunction with bacterial component of the disease warrants consideration of novel treatment approaches targeting both host immunity and pathogenic microbiome in HS.

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Altered Skin and Gut Microbiome in Hidradenitis Suppurativa

Cited by 49 publications

References 81 publications

Hyperhidrosis treatments in hidradenitis suppurativa: A systematic review

Hyperhidrosis treatments in hidradenitis suppurativa: A systematic review

A high-risk gut microbiota configuration associates with fatal hyperinflammatory immune and metabolic responses to SARS-CoV-2

Innate immunity and microbial dysbiosis in hidradenitis suppurativa – vicious cycle of chronic inflammation

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