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Oral administration of Lactococcus lactis subsp. lactis JCM5805 enhances lung immune response resulting in protection from murine parainfluenza virus infection.

Jounai K, Sugimura T, Ohshio K, Fujiwara D - PLoS ONE (2015)

Bottom Line: Microscopic observations showed that JCM5805 was incorporated into CD11c+ immune cells in Peyer's patches (PP) and PP pDCs were significantly activated and the expression levels of IFNs were significantly increased.This might be due to increased ratio of pDCs located in lung were significantly increased in JCM5805 group.Taken together, a specific LAB strain might be able to affect anti-viral immunological profile in lung via activation of intestinal pDC leading to enhanced anti-viral phenotype in vivo.

View Article: PubMed Central - PubMed

Affiliation: Technical Deveropment Center, Koiwai Dairy Products Co Ltd. Sayama, Japan; Central Laboratories for Key Technologies, Kirin Co. Ltd., Yokohama, Japan.

ABSTRACT
When activated by viral infection, plasmacytoid dendritic cells (pDCs) play a primary role in the immune response through secretion of IFN-α. Lactococcus lactis subsp. lactis JCM5805 (JCM5805) is a strain of lactic acid bacteria (LAB) that activates murine and human pDCs to express type I and type III interferons (IFNs). JCM5805 has also been shown to activate pDCs via a Toll-like receptor 9 (TLR9) dependent pathway. In this study, we investigated the anti-viral effects of oral administration of JCM5805 using a mouse model of murine parainfluenza virus (mPIV1) infection. JCM5805-fed mice showed a drastic improvement in survival rate, prevention of weight loss, and reduction in lung histopathology scores compared to control mice. We further examined the mechanism of anti-viral effects elicited by JCM5805 administration using naive mice. Microscopic observations showed that JCM5805 was incorporated into CD11c+ immune cells in Peyer's patches (PP) and PP pDCs were significantly activated and the expression levels of IFNs were significantly increased. Interestingly, nevertheless resident pDCs at lung were not activated and expressions levels of IFNs at whole lung tissue were not influenced, the expressions of anti-viral factors induced by IFNs, such as Isg15, Oasl2, and Viperin, at lung were up-regulated in JCM5805-fed mice compared to control mice. Therefore expressed IFNs from intestine might be delivered to lung and IFN stimulated genes might be induced. Furthermore, elevated expressions of type I IFNs from lung lymphocytes were observed in response to mPIV1 ex vivo stimulation in JCM5805-fed mice compared to control. This might be due to increased ratio of pDCs located in lung were significantly increased in JCM5805 group. Taken together, a specific LAB strain might be able to affect anti-viral immunological profile in lung via activation of intestinal pDC leading to enhanced anti-viral phenotype in vivo.

No MeSH data available.


Related in: MedlinePlus

Effects of JCM5805 on mPIV1 infection.A. Experimental procedure of mPIV1 infection. Mice in the control and JCM5805 groups were fed diet with or without 1 mg / mouse / day of JCM5808 during the study period (day -14 to 15). Mice were intranasally infected with mPIV1 on day 0. On 3 days post-mPIV1 infection, six mice were sacrificed from each group for lung histopathology. Thereafter survival rate, body weight and clinical scores were investigated with remained control mice n = 12, and JCM5805 mice n = 13. B. Survival rate of mice infected with mPIV1. The control (circle) and JCM5805 (square) groups consisted of 12 and 13 mice, respectively. The survival of each animal was monitored daily. P<0.001 (Log-Rank test). C. Body weight of mice infected with mPIV1. The control (circle) and JCM5805 (square) groups consisted of 12 and 13 mice, respectively. The body weight of each surviving animal was measured daily. The body weight values are shown as mean ± SD. *P<0.05, **P<0.01 (Student’s t test). The data shown is representative of two independent experiments.
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pone.0119055.g001: Effects of JCM5805 on mPIV1 infection.A. Experimental procedure of mPIV1 infection. Mice in the control and JCM5805 groups were fed diet with or without 1 mg / mouse / day of JCM5808 during the study period (day -14 to 15). Mice were intranasally infected with mPIV1 on day 0. On 3 days post-mPIV1 infection, six mice were sacrificed from each group for lung histopathology. Thereafter survival rate, body weight and clinical scores were investigated with remained control mice n = 12, and JCM5805 mice n = 13. B. Survival rate of mice infected with mPIV1. The control (circle) and JCM5805 (square) groups consisted of 12 and 13 mice, respectively. The survival of each animal was monitored daily. P<0.001 (Log-Rank test). C. Body weight of mice infected with mPIV1. The control (circle) and JCM5805 (square) groups consisted of 12 and 13 mice, respectively. The body weight of each surviving animal was measured daily. The body weight values are shown as mean ± SD. *P<0.05, **P<0.01 (Student’s t test). The data shown is representative of two independent experiments.

Mentions: mPIV1 infection of the mouse lung causes pathological lesions leading to lethality [25]. The mouse mPIV1 infection model was used to study the effect of JCM5805 on viral infection by feeding a diet containing JCM5805 starting 14 days before mPIV1 infection (Fig. 1A). Six mice from the control and JCM5805 groups were sacrificed anesthetically 3 days after infection and the lungs were isolated to examine histopathology.


Oral administration of Lactococcus lactis subsp. lactis JCM5805 enhances lung immune response resulting in protection from murine parainfluenza virus infection.

Jounai K, Sugimura T, Ohshio K, Fujiwara D - PLoS ONE (2015)

Effects of JCM5805 on mPIV1 infection.A. Experimental procedure of mPIV1 infection. Mice in the control and JCM5805 groups were fed diet with or without 1 mg / mouse / day of JCM5808 during the study period (day -14 to 15). Mice were intranasally infected with mPIV1 on day 0. On 3 days post-mPIV1 infection, six mice were sacrificed from each group for lung histopathology. Thereafter survival rate, body weight and clinical scores were investigated with remained control mice n = 12, and JCM5805 mice n = 13. B. Survival rate of mice infected with mPIV1. The control (circle) and JCM5805 (square) groups consisted of 12 and 13 mice, respectively. The survival of each animal was monitored daily. P<0.001 (Log-Rank test). C. Body weight of mice infected with mPIV1. The control (circle) and JCM5805 (square) groups consisted of 12 and 13 mice, respectively. The body weight of each surviving animal was measured daily. The body weight values are shown as mean ± SD. *P<0.05, **P<0.01 (Student’s t test). The data shown is representative of two independent experiments.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4352084&req=5

pone.0119055.g001: Effects of JCM5805 on mPIV1 infection.A. Experimental procedure of mPIV1 infection. Mice in the control and JCM5805 groups were fed diet with or without 1 mg / mouse / day of JCM5808 during the study period (day -14 to 15). Mice were intranasally infected with mPIV1 on day 0. On 3 days post-mPIV1 infection, six mice were sacrificed from each group for lung histopathology. Thereafter survival rate, body weight and clinical scores were investigated with remained control mice n = 12, and JCM5805 mice n = 13. B. Survival rate of mice infected with mPIV1. The control (circle) and JCM5805 (square) groups consisted of 12 and 13 mice, respectively. The survival of each animal was monitored daily. P<0.001 (Log-Rank test). C. Body weight of mice infected with mPIV1. The control (circle) and JCM5805 (square) groups consisted of 12 and 13 mice, respectively. The body weight of each surviving animal was measured daily. The body weight values are shown as mean ± SD. *P<0.05, **P<0.01 (Student’s t test). The data shown is representative of two independent experiments.
Mentions: mPIV1 infection of the mouse lung causes pathological lesions leading to lethality [25]. The mouse mPIV1 infection model was used to study the effect of JCM5805 on viral infection by feeding a diet containing JCM5805 starting 14 days before mPIV1 infection (Fig. 1A). Six mice from the control and JCM5805 groups were sacrificed anesthetically 3 days after infection and the lungs were isolated to examine histopathology.

Bottom Line: Microscopic observations showed that JCM5805 was incorporated into CD11c+ immune cells in Peyer's patches (PP) and PP pDCs were significantly activated and the expression levels of IFNs were significantly increased.This might be due to increased ratio of pDCs located in lung were significantly increased in JCM5805 group.Taken together, a specific LAB strain might be able to affect anti-viral immunological profile in lung via activation of intestinal pDC leading to enhanced anti-viral phenotype in vivo.

View Article: PubMed Central - PubMed

Affiliation: Technical Deveropment Center, Koiwai Dairy Products Co Ltd. Sayama, Japan; Central Laboratories for Key Technologies, Kirin Co. Ltd., Yokohama, Japan.

ABSTRACT
When activated by viral infection, plasmacytoid dendritic cells (pDCs) play a primary role in the immune response through secretion of IFN-α. Lactococcus lactis subsp. lactis JCM5805 (JCM5805) is a strain of lactic acid bacteria (LAB) that activates murine and human pDCs to express type I and type III interferons (IFNs). JCM5805 has also been shown to activate pDCs via a Toll-like receptor 9 (TLR9) dependent pathway. In this study, we investigated the anti-viral effects of oral administration of JCM5805 using a mouse model of murine parainfluenza virus (mPIV1) infection. JCM5805-fed mice showed a drastic improvement in survival rate, prevention of weight loss, and reduction in lung histopathology scores compared to control mice. We further examined the mechanism of anti-viral effects elicited by JCM5805 administration using naive mice. Microscopic observations showed that JCM5805 was incorporated into CD11c+ immune cells in Peyer's patches (PP) and PP pDCs were significantly activated and the expression levels of IFNs were significantly increased. Interestingly, nevertheless resident pDCs at lung were not activated and expressions levels of IFNs at whole lung tissue were not influenced, the expressions of anti-viral factors induced by IFNs, such as Isg15, Oasl2, and Viperin, at lung were up-regulated in JCM5805-fed mice compared to control mice. Therefore expressed IFNs from intestine might be delivered to lung and IFN stimulated genes might be induced. Furthermore, elevated expressions of type I IFNs from lung lymphocytes were observed in response to mPIV1 ex vivo stimulation in JCM5805-fed mice compared to control. This might be due to increased ratio of pDCs located in lung were significantly increased in JCM5805 group. Taken together, a specific LAB strain might be able to affect anti-viral immunological profile in lung via activation of intestinal pDC leading to enhanced anti-viral phenotype in vivo.

No MeSH data available.


Related in: MedlinePlus