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Lipooligosaccharide-deficient Neisseria meningitidis shows altered pilus-associated characteristics
Barbara Albiger1, Linda Johansson, Ann-Beth Jonsson
1Microbiology and Tumor Biology Center, Karolinska Institutet, SE-171 77 Stockholm, Sweden. Barbara.Albiger@mtc.ki.se
Abstract:
Molecular interaction between host mucosal surfaces and outer membrane components of microbes is crucial in the infection process. The outer membrane of pathogenic Neisseria contains surface molecules such as pili, PilC, and Opa and a monolayer of lipooligosaccharide (LOS), all of which are involved in the interaction with host cells. Pili mediate the initial attachment to human epithelial cells, which is followed by tight contact between bacteria and the eucaryotic cells, leading to bacterial invasion. To further examine the basis for bacterium-host cell contact, we constructed an LOS-deficient Neisseria meningitidis serogroup C mutant. LOS deficiency was without exception accompanied by altered colony opacity and morphology, which most likely represented an "on" switch for Opa540 expression, and by reduced levels of the iron-regulated proteins FetA and FbpA. We show here that LOS is essential for pilus-associated adherence but dispensable for fiber formation and twitching motility. The absence of attachment to epithelial cells could not be attributed to altered levels of piliation or defects in the pilus adhesion phenotype. Further, LOS mutants do not invade host cells and have lost the natural competence for genetic transformation.
Insights
Lipooligosaccharide (LOS) is essential for pathogenic Neisseria adherence to host cells and subsequent invasion. LOS deficiency impairs bacterial attachment and genetic transformation, highlighting its critical role in infection.
Area of Science:
- Microbiology
- Pathogenesis
- Molecular Biology
Background:
- Host-microbe molecular interactions are key in infection.
- Pathogenic Neisseria outer membrane components like pili and lipooligosaccharide (LOS) mediate host cell interactions.
- Pili facilitate initial bacterial attachment, leading to invasion.
Purpose of the Study:
- To investigate the role of lipooligosaccharide (LOS) in Neisseria meningitidis serogroup C infection.
- To elucidate the function of LOS in bacterial adherence, invasion, and genetic transformation.
Main Methods:
- Construction of a LOS-deficient Neisseria meningitidis serogroup C mutant.
- Analysis of colony morphology, Opa540 expression, and iron-regulated proteins (FetA, FbpA).
- Assessment of pilus-mediated adherence, fiber formation, twitching motility, host cell invasion, and natural competence.
Main Results:
- LOS deficiency altered colony opacity and morphology, upregulating Opa540 expression.
- LOS is essential for pilus-associated adherence but not for pilus fiber formation or twitching motility.
- LOS mutants exhibited reduced attachment to epithelial cells, lacked invasion capability, and lost natural competence.
Conclusions:
- Lipooligosaccharide (LOS) is crucial for pilus-mediated adherence and host cell invasion by pathogenic Neisseria.
- LOS plays a significant role in maintaining the pathogenic potential of Neisseria.
- Disruption of LOS impacts multiple bacterial functions, including adhesion and genetic transformation.