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Abstract:
Urinary tract infection (as apposed to symptomless bacteriuria) begins with the binding of the bacterium to the epithelium lining the urinary tract. Immune SIgA2 may react with the bacterial ligands ("adhesins") thus blocking their attachment to the epithelium. In the absence of the protective blockade tissue lesions ensues. The pathomechanism of the circumscript interstitial inflammatory spots is assumed to depend on complement activation by immune complexes of bacterial antigens and antibodies: chemotactic activity is generated from the C-system, leucocytes are attracted and the lysosomal enzymes initiate tissue damage.