Research Progress on the Correlation between Infection and Psoriasis

Psoriasis is a common cause of chronic inflammatory skin disease with unclear pathogenesis. In recent years, more and more researchers have found that infectious factors play an important role in the development of psoriasis. This article reviews the role of streptococcus, Staphylococcus aureus, and Malassezia in the development of psoriasis.

The clinical heterogeneity of psoriasis and obvious multi-gene inheritance indicate that the combination of many factors participates in its development, including genetic factors, infection, stress, environmental factors such as drugs and immune factors. Infection has long been considered a triggering or aggravating factor for psoriasis. An increase in the secretion of IL-17 leads to an imbalance of Th17/Treg, which is one of the important causes of autoimmune diseases. Some scholars believe that psoriasis is an autoimmune disease that aids in Th1/Th2 imbalance. Mucosal and systemic overexpression of pro-inflammatory Th1 cytokines and low-anti-inflammatory Th2 cytokines occur in psoriasis. Maintenance and recurrence play a role, and network imbalance of inflammatory mediators and cytokines plays an important role in the development of chronic plaque psoriasis. In recent years, the role of microorganisms in the occurrence and development of psoriasis has attracted more and more scholars’ attention. At present, scholars generally believe that microbes can participate in the occurrence and development of psoriasis by affecting the host’s immune system and gene expression. This article will review the role of streptococcus, Staphylococcus aureus, and Malassezia in the development of psoriasis from an immunological and genetic perspective.

1. Streptococcal infection

Streptococcus is a member of the family Streptococcus, and is classified into type A (type) hemolytic streptococcus, type B (β type) hemolytic streptococcus, and type C (γ type) hemolytic streptococcus according to hemolysis ability. . Streptococcus has a strong invasive ability, can produce a variety of invasive enzymes and exotoxin (M protein LTA hemolysin, etc.). With the in-depth study of the etiology and mechanism of psoriasis, an important factor in the pathogenesis of acute psoriasis: streptococcal infection has been widely recognized. In recent years, domestic researchers have found that tonsil streptococcal infection is involved in the occurrence and development of psoriasis, but its potential immunological pathogenesis has not yet been clarified. Some scholars have monitored peripheral blood cells and psoriatic lesions in patients with psoriasis. Streptococcus can produce superantigens such as streptococcal M protein and keratin to directly activate T cells to participate in the occurrence of psoriasis.

Studies have reported that patients with psoriasis are infected with streptococcus (β-hemolytic streptococcus) significantly higher than normal people, and the activation of T lymphocytes in the immune system of patients with psoriasis and streptococcus infection can be found in large numbers (CD4). And cytokines such as CD8 and IL-17 and IL-23), high expression of CLAIL-23 receptor can promote the outing of tonsil-effect T cells, and then induce or aggravate psoriasis. The human antimicrobial peptide LL-37 peptide has been shown to be an element in the regulation of innate immune responses in psoriasis, which activates CD14CD16 in patients with punctate psoriasis and activates the immune system. IL-37 peptide can cause T cell proliferation and Th17 polarization induction. Studies have shown that CD14 and CD16 in patients with psoriasis are positively correlated with the severity of psoriasis, suggesting that IL-37 peptide plays an important role in the pathogenesis of psoriasis. Peptidoglycan (PGN) is a major component of the cell wall of streptococcus. In recent years, some scholars have found that there are a large number of cells containing PGN in the lesions of patients with psoriasis. It has been reported that Gram-positive streptococci can activate the innate immune cells through the toll-like receptor (TLR) 2 and TLR4 to participate in the development and development of arthritic psoriasis. Some foreign researchers have found that the IL-17A inducer ZC3H12A encodes the ribonuclease MCPIP1 through the mouse psoriatic lesion model. The protein level of MCPIP1 encoding transcription is significantly higher than that of normal lesions. It has been reported that the expression of the causative gene HLA-Cw6 and activated lymphoid T cells and their production of Th1, Th17, Th22, IL-17A, IFN-γ, IL-17F can be found in the epidermis of the psoriasis infection. Such cytokines, as well as epidermal cell mediators (CX-CL8, CXCL9, CXCL10, CXCL11), activate Th17 cells and are directly involved in the development of psoriasis. CCL3 can participate in the development of psoriasis by regulating the level of FOXP3. FryL and other studies have found that patients with Crohn’s disease are more susceptible to psoriasis than normal people. Patients with psoriasis are more susceptible to Crohn’s disease than normal people. A large number of thick walls can be found in the intestinal microbiota of patients with Crohn’s disease. Fungi, Streptococcus, which activate the cellular innate immune system and participate in the development of psoriasis.

Some scholars have found that there are various bacterial values in the skin parts of psoriasis lesions and normal skin. Through biopsy specimens, it can be found that the most common form of patients with psoriasis is the genus Streptococcus, which is deeply studied in genetics. It was found that its genetic locus is related to the innate immune system, and psoriasis and Crohn’s disease share a common susceptibility locus. Some foreign scholars have observed and studied the psoriasis patients who have removed tonsils. The cure and effective rate of patients with psoriasis after surgical removal of tonsils are significantly higher than those of patients who have not been removed.

2. Staphylococcus aureus

Staphylococcus aureus is the most common pathogen in human purulent infections. It is a conditional pathogen on the surface of human body. The host defense mechanism of Staphylococcus aureus is not fully understood. Some researchers have found that Staphylococcus aureus colonized on the surface of patients with psoriasis has more surface than normal skin and that patients with psoriasis are more likely to colonize Staphylococcus aureus. Long-term colonization of Staphylococcus aureus on the skin surface can increase skin inflammation. The probability of occurrence and aggravation of psoriasis. Some scholars have reported that the Th17 cell pathway has less effect on Staphylococcus aureus and has lower protection on its own skin mucosa. SedefGJ uses PCR to isolate a large number of Staphylococcus aureus pathogenic factors from the lesions of patients with psoriasis. Toxins, which are statistically significant compared to healthy controls, suggest that enterotoxin produced by S. aureus may be an important factor in the exacerbation of psoriasis. MylesIA et al found that IL-19, IL-20, IL-24 and other cytokines can promote the infection of Staphylococcus aureus in mice skin, and down-regulate IL-1β and IL-17A pathway. Human keratinocytes produce some antimicrobial peptides and proteins (AMP) that protect the skin from infection. In recent years, it has been found that the cytokine IL-17A/TNF-α is a potent AMP inducer combination. Some foreign researchers have found that cIAP-2 can inhibit the anti-apoptosis of S. aureus PGN keratinocytes, and then promote the proliferation and differentiation of psoriatic keratinocytes. In genetics, foreign researchers have found that the SLURPI gene regulates the inflammatory cytokines IL-17, IL-22 production and TNF-α in a psoriasis mouse model. SLURP1 may be an important factor in psoriasis. A factor of proliferation and differentiation of keratinocytes, which significantly inhibits the growth of S. aureus.

3. Malassezia infection

Malassezia is a lipophilic fungus. Most of the bacteria contain lipase. They are embedded in the cell wall and/or cell membrane system rich in dextran. Lipase decomposes lipids into fatty acids and provides their own metabolism. The essential nutrient source is mainly parasitic on the rich parts of human sebaceous glands such as chest, back, head, face and neck. It is a conditional pathogen. The lipophilic component and hydrophilic component contained in Malassezia can induce the release of IL-8 from the host cell to activate the complement system, induce the migration of host immune cells to the dermis, and the hydrophobic component can make Th1/Th2 in the peripheral blood of the host. Induces the onset and deterioration of psoriasis. Malassezia parasitic on normal skin induces host production of transforming growth factor-β1, interleukin IL-10, inhibition of host pro-inflammatory cytokines IL-1, IL-6 and TNF-α production. Therefore, it can coexist on the host skin for a long time; on the skin damaged by the barrier, Malassezia can promote the inflammatory reaction of the cells and promote the excessive proliferation of human epithelial cells. HBD can inhibit the microbial infection by regulating the high expression of HBD-2. IL-1, IL-2, IL-6, IL-8, IL-12 and other cytokines can induce high expression of HBD-2. Foreign scholars analyzed the genetic polymorphism of the HBD region of chromosome 8 in patients with psoriasis and normal controls, and found that the expression of HBD-2 gene in patients with psoriasis was significantly higher than that in the control group. James AG et al found that the expression of HBD-2 and TNF-α in psoriatic lesions was significantly higher than that of normal skin, and increased with the severity of psoriasis, which was significant with the psoriasis PA-SI score. Positive correlation, it is speculated that Malassezia plays an important role in the occurrence and development of psoriasis. The early clinical manifestations of some patients with psoriasis may be increased dandruff. Malassezia globosa and Malassezia malforma are the main predisposing factors for dandruff increase. Some scholars believe that Malassezia globosa and Malassezia restricted It is the dominant species in psoriatic lesions. Malassezia can stimulate keratinocyte proliferation through intracellular Toll-like receptors or Nod-like receptor signaling pathways, which is related to the occurrence of psoriasis. . Early use of antifungal drugs for the treatment of psoriasis with malachite infection in lesions with only scalp areas can inhibit the development of lesions in psoriasis, but the mechanism of treatment is not yet clear and further research is needed. MattozziC et al. proposed that ketoconazole may help to improve the condition of psoriasis patients with Malassezia infection, which has been recognized by most scholars in Europe.

4. Conclusion

In summary, through immunology and genetics research, it has been proved that streptococcus, Staphylococcus aureus and Malassezia are involved in the occurrence and development of psoriasis. Anti-infective treatment can shorten the course of disease and improve the quality of life of patients. The treatment of psoriasis has guiding significance. At present, other microorganisms (virus, Mycobacterium tuberculosis, non-tuberculous mycobacteria, etc.) have been studied at home and abroad, but there are few reports. Researchers can further explore the mechanism of the occurrence and development of psoriasis complicated infection from the treatment of psoriasis, and further explore the immune mechanism induced by microbial infection or aggravate the condition of psoriasis.

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