Environmental microbes can trigger autoimmune responses through multiple pathways, and one mechanism is antigenic mimicry. We recently reported that a mimicry epitope for cardiac myosin heavy chain (Myhc)-α 334-352, designated BAC 25-40, from Bacillus sp. NRRL B-14911 can induce myocarditis in A/J mice by generating cross-reactive T cells for cardiac myosin. By 16S rRNA phylogenetic analysis, we determined the species to be Bacillus infantis NRRL B-14911. Since this microbe was originally isolated from ocean water, we sought to evaluate the expression of N-carbomoyl L-amino acid amidohydrolase (NCAA), the source protein for BAC 25-40, under various growth conditions.  Unexpectedly,  NCAA was found to be expressed in low-salt conditions when bacteria were grown at 37^oC, but not in high salt-containing marine medium, suggesting that the conditions of mammalian systems may favor the expression of NCAA in this bacterium.  Furthermore, we demonstrate that RAW 264.7 cells can phagocytose the bacteria and produce reactive oxygen- and nitrogen intermediaries to levels comparable to lipopolysaccharide.  Likewise, primary macrophages obtained from A/J mice can produce proinflammatory cytokines, notably, tumor necrosis factor-α, and interleukin-6 in response to bacterial exposure.  More importantly, A/J mice infected with B. infantis show the generation of CD4 T cells that cross-react with both BAC 25-40, and Myhc-α 334-352, as evaluated by major histocompatibility complex class II dextramer staining. Together, the data suggest that B. infantis may have a potential to induce myocarditis. The establishment of this disease model enables the study of the immune mechanisms of myocardial injuries of bacterial origin.