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Impact of Gastrointestinal Bacillus anthracis Infection on Hepatic B Cells.

Colliou N, Sahay B, Zadeh M, Owen JL, Mohamadzadeh M - Toxins (Basel) (2015)

Bottom Line: Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells.Accumulation of these cells in the liver was associated with an increase in chemokine expression.Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA. collioun@ufl.edu.

ABSTRACT
Ingestion of Bacillus anthracis results in rapid gastrointestinal (GI) infection, known as GI anthrax. We previously showed that during GI anthrax, there is swift deterioration of intestinal barrier function leading to translocation of gut-associated bacteria into systemic circulation. Additionally, we described dysfunction in colonic B cells. In concordance with our previous studies, here, we report early migration of the Sterne strain of B. anthracis along with other gut-resident bacteria into the infected murine liver. Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells. Both of these cell types are capable of producing immunoglobulins against common pathogens and commensals, which act as a general antibody barrier before an antigen-specific antibody response. Accumulation of these cells in the liver was associated with an increase in chemokine expression. These data suggest that the presence of Sterne and other commensals in the liver trigger migration of MZ-like B cells from the spleen to the liver to neutralize systemic spread. Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.

No MeSH data available.


Related in: MedlinePlus

Sterne infection changes the percentage of ILC2s in infected livers. A/J mice (n = 43) were infected with 109 spores of B. anthracis Sterne. Liver leukocytes were isolated from mice (day 1, n = 10; day 2, n = 10, day 3, n = 10; day 5 n = 13) at each indicated time point using Percoll gradients, as described in the Experimental Section. Isolated leukocytes were stained with different sets of antibodies, as depicted in the Figure S1 to define: (A) ILC2s; (B) ILC3s; (C) IL-5 producing; and (D) IL-13 producing ILC2s. Data are shown as mean ± SEM. *p < 0.05, ** <0.01, ***p < 0.001 compared with PBS-treated or day 0 mice.
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toxins-07-03805-f004: Sterne infection changes the percentage of ILC2s in infected livers. A/J mice (n = 43) were infected with 109 spores of B. anthracis Sterne. Liver leukocytes were isolated from mice (day 1, n = 10; day 2, n = 10, day 3, n = 10; day 5 n = 13) at each indicated time point using Percoll gradients, as described in the Experimental Section. Isolated leukocytes were stained with different sets of antibodies, as depicted in the Figure S1 to define: (A) ILC2s; (B) ILC3s; (C) IL-5 producing; and (D) IL-13 producing ILC2s. Data are shown as mean ± SEM. *p < 0.05, ** <0.01, ***p < 0.001 compared with PBS-treated or day 0 mice.

Mentions: Previously we have reported the depletion of ILC2s in the gut of Sterne-infected mice [10]. To evaluate whether a similar depletion can be seen in the liver, we evaluated the number of ILC2s in the liver parenchyma (Figure S1). Surprisingly, instead of a depletion, we found a significant increase in the ILC2 population during the early stage of the disease; this increase was no longer apparent at day five post-infection (Figure 4A). Bacterial infections can be efficiently cleared by ILC3s, which secrete IL-17 and recruit neutrophils [31]; upon investigation, these cells did not significantly change in their percentage within the liver during infection (Figure 4B). The cytokines produced by ILC2s were also altered during the course of infection. IL-5 and IL-13 are two major cytokines produced by ILC2s to skew the immune response towards a Th2 phenotype. During Sterne infection, IL-5 expression was maintained at early stages of the disease; however, at day three post-infection, its expression declined, suggesting limited support to B cells for their survival and maintenance at Sterne-infected hepatic loci (Figure 4C). On the other hand, IL-13 expression declined very sharply in ILC2s; nonetheless, ILC2s recovered their IL-13 expression at day five post-infection (Figure 4D).


Impact of Gastrointestinal Bacillus anthracis Infection on Hepatic B Cells.

Colliou N, Sahay B, Zadeh M, Owen JL, Mohamadzadeh M - Toxins (Basel) (2015)

Sterne infection changes the percentage of ILC2s in infected livers. A/J mice (n = 43) were infected with 109 spores of B. anthracis Sterne. Liver leukocytes were isolated from mice (day 1, n = 10; day 2, n = 10, day 3, n = 10; day 5 n = 13) at each indicated time point using Percoll gradients, as described in the Experimental Section. Isolated leukocytes were stained with different sets of antibodies, as depicted in the Figure S1 to define: (A) ILC2s; (B) ILC3s; (C) IL-5 producing; and (D) IL-13 producing ILC2s. Data are shown as mean ± SEM. *p < 0.05, ** <0.01, ***p < 0.001 compared with PBS-treated or day 0 mice.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4591657&req=5

toxins-07-03805-f004: Sterne infection changes the percentage of ILC2s in infected livers. A/J mice (n = 43) were infected with 109 spores of B. anthracis Sterne. Liver leukocytes were isolated from mice (day 1, n = 10; day 2, n = 10, day 3, n = 10; day 5 n = 13) at each indicated time point using Percoll gradients, as described in the Experimental Section. Isolated leukocytes were stained with different sets of antibodies, as depicted in the Figure S1 to define: (A) ILC2s; (B) ILC3s; (C) IL-5 producing; and (D) IL-13 producing ILC2s. Data are shown as mean ± SEM. *p < 0.05, ** <0.01, ***p < 0.001 compared with PBS-treated or day 0 mice.
Mentions: Previously we have reported the depletion of ILC2s in the gut of Sterne-infected mice [10]. To evaluate whether a similar depletion can be seen in the liver, we evaluated the number of ILC2s in the liver parenchyma (Figure S1). Surprisingly, instead of a depletion, we found a significant increase in the ILC2 population during the early stage of the disease; this increase was no longer apparent at day five post-infection (Figure 4A). Bacterial infections can be efficiently cleared by ILC3s, which secrete IL-17 and recruit neutrophils [31]; upon investigation, these cells did not significantly change in their percentage within the liver during infection (Figure 4B). The cytokines produced by ILC2s were also altered during the course of infection. IL-5 and IL-13 are two major cytokines produced by ILC2s to skew the immune response towards a Th2 phenotype. During Sterne infection, IL-5 expression was maintained at early stages of the disease; however, at day three post-infection, its expression declined, suggesting limited support to B cells for their survival and maintenance at Sterne-infected hepatic loci (Figure 4C). On the other hand, IL-13 expression declined very sharply in ILC2s; nonetheless, ILC2s recovered their IL-13 expression at day five post-infection (Figure 4D).

Bottom Line: Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells.Accumulation of these cells in the liver was associated with an increase in chemokine expression.Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA. collioun@ufl.edu.

ABSTRACT
Ingestion of Bacillus anthracis results in rapid gastrointestinal (GI) infection, known as GI anthrax. We previously showed that during GI anthrax, there is swift deterioration of intestinal barrier function leading to translocation of gut-associated bacteria into systemic circulation. Additionally, we described dysfunction in colonic B cells. In concordance with our previous studies, here, we report early migration of the Sterne strain of B. anthracis along with other gut-resident bacteria into the infected murine liver. Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells. Both of these cell types are capable of producing immunoglobulins against common pathogens and commensals, which act as a general antibody barrier before an antigen-specific antibody response. Accumulation of these cells in the liver was associated with an increase in chemokine expression. These data suggest that the presence of Sterne and other commensals in the liver trigger migration of MZ-like B cells from the spleen to the liver to neutralize systemic spread. Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.

No MeSH data available.


Related in: MedlinePlus