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, 6 (6), e21133

Nontypable Haemophilus Influenzae Displays a Prevalent Surface Structure Molecular Pattern in Clinical Isolates

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Nontypable Haemophilus Influenzae Displays a Prevalent Surface Structure Molecular Pattern in Clinical Isolates

Pau Martí-Lliteras et al. PLoS One.

Abstract

Non-typable Haemophilus influenzae (NTHi) is a gram negative pathogen that causes acute respiratory infections and is associated with the progression of chronic respiratory diseases. Previous studies have established the existence of a remarkable genetic variability among NTHi strains. In this study we show that, in spite of a high level of genetic heterogeneity, NTHi clinical isolates display a prevalent molecular feature, which could confer fitness during infectious processes. A total of 111 non-isogenic NTHi strains from an identical number of patients, isolated in two distinct geographical locations in the same period of time, were used to analyse nine genes encoding bacterial surface molecules, and revealed the existence of one highly prevalent molecular pattern (lgtF+, lic2A+, lic1D+, lic3A+, lic3B+, siaA-, lic2C+, ompP5+, oapA+) displayed by 94.6% of isolates. Such a genetic profile was associated with a higher bacterial resistance to serum mediated killing and enhanced adherence to human respiratory epithelial cells.

Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Schematic representation of NTHi LOS structure.
Relevant sugars linked by the products from the genes lgtF, lic2C, lpsA, lic3A, lic3B, siaA, lsgB, lic1ABCD, lic2A, lgtC and lex2B are shown. Abbreviations: Kdo, 2-keto-3-deoxyoctulosonic acid; Hep, L-glycero-D-manno-heptose; Glc, D-glucose; Gal, D-galactose; PEtn, phosphoethanolamine; P, phosphate; PCho, phosphocholine. For each LOS structure the heptose backbone comprises from top to bottom HepI, HepII and HepIII.
Figure 2
Figure 2. Electrophoresis profiles of LOS isolated from representative NTHi strains.
LOS from representative NTHi strains were isolated and separated after SDS-PAGE; strains NTHi1500, 1559, 1560 (pattern 1); NTHi398, 1513, 1549, 1553, 1556, 1557, 1558, 1566, 1568, 1606, 1607, 1621, 1622, 1623, 1630 (pattern 2); NTHi1619 (pattern 3). A pair of profiles, before (−) and after (+) neuraminidase treatment, is shown for each strain. Arrows show bands removed or altered following neuraminidase treatment.
Figure 3
Figure 3. Adhesion of representative NTHi clinical isolates to A549 airway epithelial cells.
NTHi strains were used to infect A549 cells at an MOI of 100∶1 for 30 min. Bacterial adhesion was quantified following lysis of host cells, serial dilution, and viable counting. The level of adhesion was determined as follows: percent adhesion = (cfu output/cfu input)×100. Black bars correspond to strains with pattern 1; gray bars to strains with pattern 2; white bar to strain with pattern 3.
Figure 4
Figure 4. Adhesion of representative NTHi isolates to over-confluent A549, to HeLa-BGP and to Detroit 562 pharynx epithelial cells.
NTHi strains were used to infect (A) over-confluent A549, (B) HeLa-BGP and (C) Detroit 562 epithelial cells at an MOI of 100∶1 for 30 min. Bacterial adhesion was quantified following lysis of host cells, serial dilution, and viable counting. The level of adhesion was determined as follows: percent adhesion = (cfu output/cfu input)×100. (D) Detection of human CEACAM1 receptor in confluent A549, HeLa-BGP and Detroit 562 epithelial cells by Western Blot with mouse anti-CEACAM1 and goat anti-mouse conjugated to horseradish peroxidase antibodies (upper panel). Extracts were prepared from non-infected cells. Detection of tubulin (bottom panel) was used as control. In (A), (B) and (C), black bars correspond to strains with pattern 1; gray bars to strains with pattern 2; white bar to strain with pattern 3.

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