The nonpathogenic hrcC mutant of Xanthomonas campestris pv. vesicatoria 85-10::hrpA22 multiplied in pepper leaves if it was mixed with pathogenic strains of X. campestris pv. vesicatoria. Reactions to the mutant alone included localized deposition of phenolics and callose in papillae, and alterations to the plant cell wall leading to increased electron density. Electron microscopy showed that the localized responses were suppressed in the presence of wild-type bacteria but other wall changes occurred at some sites, involving cellulose-rich ingrowth of the wall. Multiplication of the hrp mutant in mixed inocula was confirmed by tagging 85-10::hrpA22 using immunocytochemical location of AvrBs3 expressed from the plasmid pD36. Elicitors of callose deposition and other wall changes were isolated from the hrcC mutant. Activity in extracts of bacteria was attributed to the presence of high molecular weight lipopolysaccharides (LPS). Wild-type X. campestris pv. vesicatoria suppressed induction of structural changes caused by purified LPS. Results obtained suggest that effector proteins produced by phytopathogenic bacteria and delivered by the type III secretion system may have a key role in suppressing the basal defense responses activated by bacterial LPS, which lead to restricted multiplication of nonpathogens such as hrp mutants.