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Helicobacter pylori
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===Catalase=== Colonization induces an intense anti-inflammatory response as a first-line immune system defence. Phagocytic leukocytes and monocytes infiltrate the site of infection, and antibodies are produced.<ref name="Ramarao">{{cite journal |vauthors=Ramarao N, Gray-Owen SD, Meyer TF |title=Helicobacter pylori induces but survives the extracellular release of oxygen radicals from professional phagocytes using its catalase activity |journal=Mol Microbiol |volume=38 |issue=1 |pages=103β13 |date=October 2000 |pmid=11029693 |doi=10.1046/j.1365-2958.2000.02114.x |url=|hdl=11858/00-001M-0000-000E-C7AD-8 |hdl-access=free }}</ref> ''H. pylori'' is able to adhere to the surface of the phagocytes and impede their action. This is responded to by the phagocyte in the generation and release of oxygen metabolites into the surrounding space. ''H. pylori'' can survive this response by the activity of [[catalase]] at its attachment to the phagocytic cell surface. Catalase decomposes hydrogen peroxide into water and oxygen, protecting the bacteria from toxicity. Catalase has been shown to almost completely inhibit the phagocytic oxidative response.<ref name="Ramarao" /> It is coded for by the gene ''katA''.<ref name="UniProt1">{{cite web |title=UniProt |url=https://www.uniprot.org/uniprotkb/P77872/entry |website=www.uniprot.org |access-date=20 March 2024}}</ref>
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