English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Escherichia coli strains of group O111 were characterized with respect to sensitivity to complement killing, amount of lipopolysaccharide and O antigen-containing capsule, and distribution of O antigen. All wild-type E. coli O111 strains were resistant to complement killing in the absence of specific antibody. Presensitization of strains with antibody to whole cells (OK antibody), followed by incubation in 50% pooled normal human serum as a source of complement, subdivided wild-type strains into three types: completely resistant, partially resistant, and sensitive. Completely and partially resistant mutants were isolated by cycles of serum killing, starting with one sensitive strain. Completely resistant mutants had no O antigen-containing capsule, but had 50% more lipopolysaccharide than did the parent, and this lipopolysaccharide had 30% fewer lipid A core molecules devoid of O antigen. Partially resistant mutants still had O antigen-containing capsule, but contained 40% more lipopolysaccharide than did the parent; the extent of coverage of lipid A core with O antigen remained unchanged. No correlations were found between outer membrane protein composition and the degree of serum resistance. Since the terminal membrane attack complex (C5b-9) must stably insert into a hydrophobic membrane site to effect killing, we conclude that both increased lipid A core and increased coverage of lipid A core with O antigen preclude access of C5b-9 to lethal sites on the cell surface.

journal of bacteriology

Serum-resistant mutants of Escherichia coli O111 contain increased lipopolysaccharide, lack an O antigen-containing capsule, and cover more of their lipid A core with O antigen