Infectious triggers for vasculitis.
OBJECTIVE
Infections have been suggested to contribute to disease induction and reactivation in many of the idiopathic vasculitides. This review describes and evaluates the evidence that microbes are involved in the etiopathogenesis of these diseases.


RESULTS
Large-vessel vasculitis has recently been associated with two specific bacteria. Mycobacterium tuberculosis is thought to have an inducing role in Takayasu arteritis and a Burkholderia bacterium might be involved in giant cell arteritis. Hepatitis B and C viruses have been linked to polyarteritis nodosa. In antineutrophil cytoplasmic autoantibody-associated vasculitis, and more specifically granulomatosis with polyangiitis (GPA), Staphylococcus aureus has been the focus of many studies. Chronic nasal carriage of S. aureus is related to endonasal activity and disease relapses in GPA patients. Moreover, antibacterial treatment is known to reduce the risk for disease relapses. If and how pathogens trigger vasculitis is still unclear, but several potential mechanisms have been suggested and are briefly reviewed here.


CONCLUSIONS
Although many observations suggest a link between infections and the development of vasculitis, no direct proof exists. Transcriptomic and proteomic studies of the pathogens involved could aid in identifying specific or common traits of pathogens that are relevant for the development and reactivation of vasculitis.
aDepartment of Pathology and Medical Biology bDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Mirjan M
MM
van Timmeren
Peter
P
Heeringa
Cees G M
CG
Kallenberg
D006509:Hepatitis B / Q000150:complications*; D006526:Hepatitis C / Q000150:complications*; D006801:Humans; D009164:Mycobacterium Infections / Q000150:complications*; D013203:Staphylococcal Infections / Q000150:complications*; D014657:Vasculitis / Q000209:etiology* / Q000276:immunology