Occurrence and relevance of Mycoplasma spp. in free-ranging pheasants from northwestern Germany

Since 2008/2009, the population of free-ranging ring-necked pheasants was recorded to decrease all over Germany. Various Mycoplasma (M.) spp. are causing severe respiratory signs in captive game bird species. Furthermore, M. gallisepticum is responsible for massive die-offs in consequence to severe conjunctivitis in house finches in the USA. Therefore, the prevalence of mycoplasmas in free-ranging pheasants was investigated and a potential impact on the population decline of pheasants discussed. Within this study, 150 free-ranging pheasants were sampled via tracheal swabs and tissue samples of the trachea and the periorbital skin, as the latter displayed inflammatory alterations in previous studies. In total, 177 samples were investigated for the presence of mycoplasmas using cultural and molecular biological methods. In 76 birds, necropsy was performed additionally. In total, 73.7% (51/76) of the examined pheasants had periorbital skin alterations. Furthermore, 64.4% (114/177) of the samples tested positive for mycoplasmas via PCR. Overall, 102/177 samples (57.6%, 78/105 tracheal swabs, 19/51 skin tissue, 5/21 trachea tissue) tested positive for mycoplasmas via culture. Mycoplasma gallinaceum (n = 50), M. pullorum (n = 45), M. glycophilum (n = 43), M. iners (n = 11), and M. gallinarum (n = 5) were frequently isolated. In 45 cases (45.9%), multiple Mycoplasma spp. were isolated from one sample. All examined samples tested negative for M. gallisepticum. Of 51 skin samples investigated for mycoplasmas, 24 (47.1%) showed inflammatory skin alterations in histology, and 58.3% (14/24) of these samples tested positive for Mycoplasma spp. additionally. Overall, there was a significant correlation between inflammatory altered skin samples and the detection of mycoplasmas in periorbital skin samples. Based on the present results, the isolated Mycoplasma spp. may play a role as facultative agents for the observed inflammatory skin alterations. However, additional investigation is needed to confirm this presumption.

Crosstalk between keratinocytes and immune cells in inflammatory skin diseases

Cutaneous homeostasis is maintained by dynamic cellular communications between different cell types in the skin through interactions with various mediators, including cytokines, chemokines and antimicrobial peptides/proteins (AMPs). Keratinocytes, as the major cell type of the epidermis, not only form a passive physical barrier, but also actively participate in the pathogenesis of many, if not all, inflammatory skin diseases. Keratinocytes highly interact with immune cells to shape, amplify or regulate inflammatory responses, thus triggering and/or sustaining these inflammatory skin diseases. In this review, crosstalk between keratinocytes and immune cells is summarized, and its contributions to two major inflammatory skin disorders including psoriasis and atopic dermatitis are highlighted.

The role of gut microbiome in inflammatory skin disorders: a systematic review

The close relationship between the intestine and the skin has been widely stated, seen from gastrointestinal (GI) disorders often accompanied by skin manifestations. Exactly how the gut microbiome is related to skin inflammation and influences the pathophysiology mechanism of skin disorders are still unclear. Many studies have shown a two-way relationship between gut and skin associated with GI health and skin homeostasis and allostasis. This systematic review aimed to explore the associations between the gut microbiome with inflammatory skin disorders, such as acne, psoriasis, atopic dermatitis, and urticaria, and to discover the advanced concept of this relationship. Methods: The literature search was limited to any articles published up to December 2020 using PubMed and EBSCOHost. The review followed the PRISMA guidelines for conducting a systematic review. Result: Of the 319 articles screened based on title and abstract, 111 articles underwent full-text screening. Of these, 23 articles met our inclusion criteria, comprising 13 AD, three psoriasis, four acne vulgaris, and four chronic urticaria articles. Discussion: Acne vulgaris, atopic dermatitis, psoriasis, and chronic urticaria are inflammation skin disorders that were studied recently to ascertain the relationship of these disorders with dysbiosis of the GI microbiome. All acne vulgaris, psoriasis, and chronic urticaria studies stated the association of gut microbiome with skin manifestations. However, the results in atopic dermatitis are still conflicting. Most of the articles agree that Bifidobacterium plays an essential role as anti-inflammation bacteria, and Proteobacteria and Enterobacteria impact inflammation in inflammatory skin disorder.

Janus Kinase Inhibitors Ameliorated Gastrointestinal Amyloidosis and Hypoalbuminemia in Persistent Dermatitis Mouse Model

Malnutrition is not only regarded as a complication of rheumatoid arthritis and inflammatory bowel disease but also that of inflammatory skin disease; however, the mechanisms and efficacy of its treatment have not been elucidated. Using a mouse model of dermatitis, we investigated the pathophysiology of malnutrition in inflammatory skin conditions and efficacy of its treatment. We employed spontaneous skin inflammation mice models overexpressing human caspase-1 in the epidermal keratinocytes. Body weight, nutrition level, and α1-antitrypsin fecal concentration were measured. The gastrointestinal tract was histologically and functionally investigated. Fluorescein isothiocyanate (FITC)-dextran was forcibly fed on an empty stomach, and plasma FITC-dextran was measured. The treatment efficacy of antibodies against tumor necrosis factor-α (TNF-α) and interleukin (IL)-α/β as well as Janus kinase (JAK) inhibitors was investigated. Compared with wild-type littermates, the inflammatory skin mice models showed a lowered body weight, reduction of serum albumin level, amyloid deposition in the stomach, small intestine, and large intestine, and increased α1-antitrypsin fecal concentration. However, the plasma FITC-dextran was unchanged between the dermatitis models and wild-type littermates. The over-produced serum amyloid A1 in the liver was detected in the plasma in the dermatitis model. Antibodies against TNF-α and IL-α/β showed partial effects on amyloid deposition; however, JAK inhibitors improved gastrointestinal amyloidosis with the improvement of skin symptoms. Chronic dermatitis is closely related to secondary amyloidosis in the gastrointestinal tract, resulting in hypoalbuminemia. Therefore, active control of skin inflammation is essential for preventing gastrointestinal complications.