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The secretion of IL-22 from mucosal NKp44⁺ NK cells is associated with microbial translocation and virus infection in SIV/SHIV-infected Chinese macaques.

Wang W, Wu F, Cong Z, Liu K, Qin C, Wei Q - J Immunol Res (2014)

Bottom Line: Microbial translocation (MT) causes systemic immune activation in chronic human immunodeficiency virus (HIV) infection.As a result, the degranulation capacity and IL-22 production of mucosal NKp44(+) NK cells were associated with the MT level in the SHIV-infected macaques.The number of mucosal NKp44(+) NK cells and interleukin-22 (IL-22) secretion by these cells increased before MT occurred.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health, Key Laboratory of Human Diseases Animal Models, State Administration of Traditional Chinese Medicine, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Comparative Medical Center, Peking Union Medical College, No. 5 Panjiayuan Nanli, Chaoyang District, Beijing 100021, China.

ABSTRACT
Microbial translocation (MT) causes systemic immune activation in chronic human immunodeficiency virus (HIV) infection. The role of a novel subtype of innate lymphoid cells, the NKp44(+) NK cells, in HIV/simian immunodeficiency virus- (SIV-) induced MT remains unknown. In this study, 12 simian-human immunodeficiency virus- (SHIV-) infected macaques were chosen and split into two groups based on the MT level. Blood and Peripheral lymphoid tissue were sampled for flow cytometric analysis, viral load detection, and interleukin testing. Then, six naive Chinese macaques were used to determine the dynamics of cytokine secretion from mucosal NKp44(+) NK cells in different phases of SIV infection. As a result, the degranulation capacity and IL-22 production of mucosal NKp44(+) NK cells were associated with the MT level in the SHIV-infected macaques. And the number of mucosal NKp44(+) NK cells and IL-22 secretion by these cells were lower in the chronic phase than in the early acute phase of SIV infection. The number of mucosal NKp44(+) NK cells and interleukin-22 (IL-22) secretion by these cells increased before MT occurred. Therefore, we conclude that a decline in IL-22 production from mucosal NKp44(+) NK cells induced by virus infection may be one of the causes of microbial translocation in HIV/SIV infection.

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Related in: MedlinePlus

Lipopolysaccharide (LPS) levels are not associated with plasma viral load (PVL), CD4+ T cells, route of infection, or virus strain. Peripheral LPS levels of infected Chinese macaques did not correlate with (a) PVL (Spearman correlation test, Rs = 0.1369), (b) peripheral CD4+ T cells (Spearman correlation test, Rs = 0.1616), (c) infectious route (two-sided nonparametric Mann-Whitney U test, P = 0.9095), or (d) virus strain (two-sided nonparametric Mann-Whitney U test, P = 0.5075).
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fig1: Lipopolysaccharide (LPS) levels are not associated with plasma viral load (PVL), CD4+ T cells, route of infection, or virus strain. Peripheral LPS levels of infected Chinese macaques did not correlate with (a) PVL (Spearman correlation test, Rs = 0.1369), (b) peripheral CD4+ T cells (Spearman correlation test, Rs = 0.1616), (c) infectious route (two-sided nonparametric Mann-Whitney U test, P = 0.9095), or (d) virus strain (two-sided nonparametric Mann-Whitney U test, P = 0.5075).

Mentions: We determined plasma viral RNA loads and peripheral CD4+ T cell count to assess set point viremia and disease progression. The results showed that the majority of Chinese macaques were in the chronic phase of SHIV infection (Table 1). The levels of neither LPS nor LBP showed a strong correlation with plasma viral RNA loads and peripheral CD4 T cell counts (Figure 1 and Figure  S1). Furthermore, the levels of LPS and LBP were not correlated with presence of infectious virus and route of infection (Figure 1 and Figure  S1). In addition, the repeated dosing of 10 animals showed a possible association with MT, but the correlation rank-order coefficient was low (Rs = 0.2059). Based on the levels of LPS and LBP, six Chinese macaques with the lowest levels of MT (MTlow) and six Chinese macaques with the highest level of MT (MThigh) were chosen from the original group of 20 (Table 1 and Figure  S1(a)) for further research. The LPS and LBP levels of the MTlow group were not significantly different from those of the naïve Chinese macaques (P = 0.066 for LPS and P = 0.568 for LBP) but were significantly lower than those of the MThigh group (P = 0.004 for LPS and P = 0.003 for LBP) (Figures  S1(b) and  S1(c)).


The secretion of IL-22 from mucosal NKp44⁺ NK cells is associated with microbial translocation and virus infection in SIV/SHIV-infected Chinese macaques.

Wang W, Wu F, Cong Z, Liu K, Qin C, Wei Q - J Immunol Res (2014)

Lipopolysaccharide (LPS) levels are not associated with plasma viral load (PVL), CD4+ T cells, route of infection, or virus strain. Peripheral LPS levels of infected Chinese macaques did not correlate with (a) PVL (Spearman correlation test, Rs = 0.1369), (b) peripheral CD4+ T cells (Spearman correlation test, Rs = 0.1616), (c) infectious route (two-sided nonparametric Mann-Whitney U test, P = 0.9095), or (d) virus strain (two-sided nonparametric Mann-Whitney U test, P = 0.5075).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4352435&req=5

fig1: Lipopolysaccharide (LPS) levels are not associated with plasma viral load (PVL), CD4+ T cells, route of infection, or virus strain. Peripheral LPS levels of infected Chinese macaques did not correlate with (a) PVL (Spearman correlation test, Rs = 0.1369), (b) peripheral CD4+ T cells (Spearman correlation test, Rs = 0.1616), (c) infectious route (two-sided nonparametric Mann-Whitney U test, P = 0.9095), or (d) virus strain (two-sided nonparametric Mann-Whitney U test, P = 0.5075).
Mentions: We determined plasma viral RNA loads and peripheral CD4+ T cell count to assess set point viremia and disease progression. The results showed that the majority of Chinese macaques were in the chronic phase of SHIV infection (Table 1). The levels of neither LPS nor LBP showed a strong correlation with plasma viral RNA loads and peripheral CD4 T cell counts (Figure 1 and Figure  S1). Furthermore, the levels of LPS and LBP were not correlated with presence of infectious virus and route of infection (Figure 1 and Figure  S1). In addition, the repeated dosing of 10 animals showed a possible association with MT, but the correlation rank-order coefficient was low (Rs = 0.2059). Based on the levels of LPS and LBP, six Chinese macaques with the lowest levels of MT (MTlow) and six Chinese macaques with the highest level of MT (MThigh) were chosen from the original group of 20 (Table 1 and Figure  S1(a)) for further research. The LPS and LBP levels of the MTlow group were not significantly different from those of the naïve Chinese macaques (P = 0.066 for LPS and P = 0.568 for LBP) but were significantly lower than those of the MThigh group (P = 0.004 for LPS and P = 0.003 for LBP) (Figures  S1(b) and  S1(c)).

Bottom Line: Microbial translocation (MT) causes systemic immune activation in chronic human immunodeficiency virus (HIV) infection.As a result, the degranulation capacity and IL-22 production of mucosal NKp44(+) NK cells were associated with the MT level in the SHIV-infected macaques.The number of mucosal NKp44(+) NK cells and interleukin-22 (IL-22) secretion by these cells increased before MT occurred.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health, Key Laboratory of Human Diseases Animal Models, State Administration of Traditional Chinese Medicine, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Comparative Medical Center, Peking Union Medical College, No. 5 Panjiayuan Nanli, Chaoyang District, Beijing 100021, China.

ABSTRACT
Microbial translocation (MT) causes systemic immune activation in chronic human immunodeficiency virus (HIV) infection. The role of a novel subtype of innate lymphoid cells, the NKp44(+) NK cells, in HIV/simian immunodeficiency virus- (SIV-) induced MT remains unknown. In this study, 12 simian-human immunodeficiency virus- (SHIV-) infected macaques were chosen and split into two groups based on the MT level. Blood and Peripheral lymphoid tissue were sampled for flow cytometric analysis, viral load detection, and interleukin testing. Then, six naive Chinese macaques were used to determine the dynamics of cytokine secretion from mucosal NKp44(+) NK cells in different phases of SIV infection. As a result, the degranulation capacity and IL-22 production of mucosal NKp44(+) NK cells were associated with the MT level in the SHIV-infected macaques. And the number of mucosal NKp44(+) NK cells and IL-22 secretion by these cells were lower in the chronic phase than in the early acute phase of SIV infection. The number of mucosal NKp44(+) NK cells and interleukin-22 (IL-22) secretion by these cells increased before MT occurred. Therefore, we conclude that a decline in IL-22 production from mucosal NKp44(+) NK cells induced by virus infection may be one of the causes of microbial translocation in HIV/SIV infection.

Show MeSH
Related in: MedlinePlus