Gut bacterial communities of diarrheic patients with indications of Clostridioides difficile infection

Gut bacterial communities of diarrheic patients with indications of Clostridioides difficile infection

We present bacterial 16S rRNA gene datasets derived from stool samples of 44 patients with diarrhea indicative of a Clostridioides difficile infection.
After processing of paired-end sequencing data, reads were merged, quality-filtered, primer sequences removed, reads truncated to 400 bp and dereplicated.
The bacterial community profiles are based on operational taxonomic unit (OTU, defined at 97% genetic identity) frequency in stool samples of 44 patients with diarrhea indicative of C. difficile infection and 35 asymptomatic control individuals (n=79).
Occurrence of diarrhea in patents is indicated by plus (patient exhibited diarrhea) and minus (no diarrhea), results from microbiological diagnosis of C. difficile infection (C. d. m. t.) are shown below (plus, positively tested for C. difficile; minus, negatively tested for C. difficile).
Full size image Non-metric multidimensional scaling (NMDS) based on weighted Unifrac12 was used to display the bacterial community structure in 79 stool samples at same sequencing effort (10.000 reads per sample).
Full size image We present bacterial 16S rRNA gene datasets derived from stool samples of 44 patients with diarrhea indicative of a Clostridioides difficile infection.
After processing of paired-end sequencing data, reads were merged, quality-filtered, primer sequences removed, reads truncated to 400 bp and dereplicated.
The bacterial community profiles are based on operational taxonomic unit (OTU, defined at 97% genetic identity) frequency in stool samples of 44 patients with diarrhea indicative of C. difficile infection and 35 asymptomatic control individuals (n=79).
Occurrence of diarrhea in patents is indicated by plus (patient exhibited diarrhea) and minus (no diarrhea), results from microbiological diagnosis of C. difficile infection (C. d. m. t.) are shown below (plus, positively tested for C. difficile; minus, negatively tested for C. difficile).
Full size image Non-metric multidimensional scaling (NMDS) based on weighted Unifrac12 was used to display the bacterial community structure in 79 stool samples at same sequencing effort (10.000 reads per sample).

Heparin at physiological concentration can enhance PEG-free in vitro infection with human hepatitis B virus

Heparin at physiological concentration can enhance PEG-free in vitro infection with human hepatitis B virus

High concentration of heparin has been commonly used as an inhibitor control for in vitro infection in the field.
However, to our surprise, at its physiological concentration (1 to 5 μg/ml), heparin could actually enhance HBV infection efficiency in both HepaRG and NTCP-reconstituted hepatocytes.
This enhancement effect of heparin could become obscured in the presence of 4% PEG, a concentration commonly used in HBV in vitro infection experiments.
Establishment of an HBV in vitro infection system using a HepG2-NTCP-AS cell line.
(d) Heparin at physiological concentrations (1 to 5 µg/ml)14,15,16 can enhance HBV infection in a dose-response experiment.
Increasing concentrations of heparin (0, 1.5, 4.5, 13.5, 40, 120 μg/ml) were used in the presence of 1.2% PEG or 4% PEG.
These HepG2-NTCP-AS cells were infected with HBV serum in the presence of 1.2% PEG with and without 4.5 μg/ml heparin.
HepG2-NTCP-AS cells were infected with HBV serum in the presence of 1.2% PEG, with and without 4.5 μg/ml heparin.
HepG2-NTCP-AS cells were infected with HBV serum pre-mixed with and without 4.5 μg/ml heparin.
(b) Heparin can further enhance HBV infection using HepaRG cells in the presence of 1.2% or 4% PEG.

Is pneumonia contagious? Causes and transmission

Is pneumonia contagious? Causes and transmission

Viruses or bacteria, which are contagious, cause most forms of pneumonia.
Both viruses and bacteria are contagious.
This makes a person more vulnerable to other types of infections.
The virus spreads easily from person to person, causing a range of symptoms and conditions.
Getting the vaccination can help prevent this type of infection from developing.
This can occur when a person with pneumonia coughs or sneezes and another person inhales the infected particles.
When a person with an infection coughs into their hand and then shakes another person’s hand, the second person can become infected if they touch their mouth or eyes without washing their hands.

Hookworm: a neglected resurgent infection

Hookworm: a neglected resurgent infection

Hookworms are a group of soil transmitted helminths included in the World Health Organization’s portfolio of neglected tropical diseases.
Ancylostoma duodenale and Necator americanus infect humans.
In addition, the primarily canine hookworm, Ancylostoma ceylanicum, is now recognised as an important cause of zoonotic disease, particularly in South East Asia.
Hookworm infection is a precipitating factor for iron deficiency anaemia as a result of blood loss proportional to the number of adult worms in the gut.1 The prevalence of infection increases with age, typically levelling off in late adolescence, while its intensity—the number of worms in a given person—generally increases throughout adulthood.
Regular anthelmintic treatment of populations where hookworm is endemic increases individuals’ haemoglobin concentrations, especially when coupled with treatment of iron deficiency anaemia.2 Globally, an estimated 472 million people are infected with hookworm, causing 4 million disability adjusted life years (DALYs), mainly from iron deficiency anaemia and its consequences, with economic productivity losses of up to $139bn (£105bn; €118bn) annually.3 Resurgence There have been reports of a possible resurgence in hookworm infection in the US, with 34% of African American …

S100A4 contributes to colitis development by increasing the adherence of Citrobacter rodentium in intestinal epithelial cells

S100A4 contributes to colitis development by increasing the adherence of Citrobacter rodentium in intestinal epithelial cells

Furthermore, C. rodentium colonization of colons in S100A4−/− mice was significantly less than those in WT mice after infection on day 7 (P < 0.05) (Fig. with C. rodentium (n = 4), *P < 0.05, **P < 0.01. In addition, the levels of anti-inflammatory cytokines IL-9 and IL-10 in S100A4−/− mice were also decreased compared to WT mice after C. rodentium infection on day 7 (P < 0.05, P < 0.01) (Fig. Inflammatory cell infiltration was impaired in S100A4−/− mice compared to WT mice after C. rodentium infection (Fig. On day 7 after C. rodentium infection, cell percentages of all analyzed myeloid cell types (F4/80+, Gr-1+) in S100A4−/− mouse colons were significantly lower than those in WT colons (P < 0.01), except for that of CD11c+ cells (Fig. We found that the p-Stat3, p-Erk levels in C. rodentium infected colon tissues in S100A4−/− mice were clearly down-regulated compared to those in WT mice (Fig. The number of bacteria counts in lamina propria of S100A4−/− mice colon was decreased compared with that in WT mice colon on day 7 (Fig. (P < 0.05).The above results indicate that S100A4 can promote the adherence of C. rodentium to CT26 cells via regulating the expression of integrin β−1. (G) Bacterial titers in fecal homogenates from AIIB2 treated WT mice and control WT mice on day 7 after C. rodentium infection (n = 5); *P < 0.05.