17 research outputs found

    Role of the social interface in consortia.

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    <p>The social interface (SI) appears to be responsible for management of the cooperation of syngeneic cells in consortia, detection of selfish/cheater behavior of syngeneic or allogeneic cells, and control and memorization of cheaters. To escape policing mechanisms of SIs, cheaters develop anticheating escape mechanisms, leading to “Red Queen” antagonistic coevolution.</p

    The relationship between the metazoan immune system and the microbial world.

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    <p><b>A.</b> In the neo-Darwinian–inspired Red Queen paradigm, the immune system (IS) fights microbial pathogens and protects the integrity of the host organism. Pathogens are identified by the presence of PAMPs and DAMPs. <b>B.</b> In the social interface paradigm, the IS allows for the establishment of a symbiotic relationship between the host and parasites and the microbiota. Discrimination is based on a cheater or cooperative profile. In this new paradigm, the organism loses its unicity and strict boundaries and becomes an open, dynamic, and mixed consortium.</p

    Characterization of infected cells expressing CD11c, CD205 and MOMA-1 in the spleen of IL12p40-deficient BALB/c mice.

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    <p>IL12p40<sup>-/-</sup> STAT6<sup>+/+</sup> BALB/c mice were injected i.n. with 2x10<sup>7</sup> CFU of mCherry-Br. The mice were sacrificed at 28 days post-infection and the spleens were collected and examined by immunohistofluorescence. <b>A</b>, The left panel shows mCherry-Br co-localization with cells expressing CD11c. The middle panel shows mCherry-Br co-localization with cells expressing CD205 and the right panel shows co-localization of CD11c- and CD205-expressing cells. <b>B</b>, The upper panels show distribution of MOMA-1-expressing cells and co-localization with mCherry-Br (left), distribution of DEC205-expressing cells and co-localization with mCherry-Br (middle), and co-localization of MOMA-1- and CD205-expressing cells (right). The panels below are higher magnification views of the same stainings. The panels are color-coded with the text for phalloidin, the antigen examined or mCherry-Br. Scale bar = 50 and 20 μm, as indicated. r.p.: red pulp; w.p.: white pulp. Yellow arrowheads indicate the presence of bacteria. The data are representative of at least two independent experiments.</p

    Analysis of CD205, Arginase1, Fizz1 and CD301 expression on infected spleen cells from IL12p40- and STAT6/IL12p40-deficient BALB/c mice.

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    <p>IL12p40<sup>-/-</sup> STAT-6<sup>+/+</sup> and IL12p40<sup>-/-</sup> STAT-6<sup>-/-</sup> BALB/c mice were injected i.n. with 2x10<sup>7</sup> CFU of mCherry-Br. The mice were sacrificed at 28 days post-infection and the spleens were collected. The figure shown the percentage of mCherry-Br that co-localizes or not with Dec205-, Arg1-, Fizz1- and CD301-expressing cells in the spleen of IL12p40<sup>-/-</sup> STAT-6<sup>+/+</sup> and IL12p40<sup>-/-</sup> STAT-6<sup>-/-</sup> BALB/c mice. The percentage of co-localization between mCherry-Br and positive cells for the antigen in IL12p40<sup>-/-</sup> STAT-6<sup>+/+</sup> mice is indicated. The data are representative of at least two independent experiments.</p

    Course of <i>B</i>. <i>melitensis</i> infection in organs of wild-type (wt), STAT6-, IL12p40- and STAT6/IL12p40-deficient BALB/c mice.

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    <p>The mice were injected intranasally (i.n.) with 2x10<sup>7</sup> CFU of mCherry-Br <i>B</i>. <i>melitensis</i> and sacrificed at the indicated times. The data represent the number of CFU per gram of lung, spleen and liver. Grey bars represent the medians. “n” is the number of mice used. These results are representative of at least two independent experiments. ns, non-significant.</p

    Characterization of the cell surface phenotype of infected cells in the spleen of IL12p40-deficient BALB/c mice.

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    <p>IL12p40<sup>-/-</sup> STAT6<sup>+/+</sup> BALB/c mice were injected i.n. with 2x10<sup>7</sup> CFU of mCherry-Br. The mice were sacrificed at 28 days post-infection and the spleens were collected and examined by immunohistofluorescence. <b>A</b>. The left panels show the overall distribution of the CD11c-, ERTR9 and MOMA-1-expressing cells in the spleen. The panels to the right of the first ones show mCherry-Br co-localization with negative cells and positive cells for CD11c, ER-TR9 and MOMA-1. The panels are color-coded with the text for phalloidin, the antigen examined or mCherry-Br. Scale bar = 200 and 20 μm, as indicated. r.p.: red pulp; w.p.: white pulp. Yellow arrowheads indicate the presence of bacteria. The data are representative of at least three independent experiments. <b>B</b>. Representative confocal images of mCherry-Br infected CD11c<sup>+</sup> cells. The panels are color-coded with the text for DAPI, mCherry-Br or CD11c. Scale bar = 10 μm, as indicated. w.p.: white pulp.</p

    image_3.tif

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    <p>Leishmania major (L. major) parasites are intracellular parasites belong to the Trypanosomatidae family and are the causative agent of cutaneous leishmaniasis. This disease affects approximately 1.5 million per year worldwide and there is currently no prophylactic vaccine available. L. major is transmitted by the bite of an infected sandfly and has been considered for decades now as a mouse model of choice to identify the factors implicated in T helper (Th)1 and Th2 polarization due to the natural resistance and susceptibility to infection of C57BL/6 and BALB/c mice, respectively. In this study, we refine the role of IL-12p40 cytokine, which is implicated the development of a protective Th1 response, and STAT6, a transcription factor involved in the signaling via detrimental interleukin (IL)-4 and IL-13 associated Th2 cytokines during L. major infection in the BALB/c model. In the absence of STAT6 and IL-12p40 signaling, double knockout (DKO) susceptible BALB/c mice displayed reduced footpad swelling and ulcerative lesion compared to IL-12p40<sup>−/−</sup> mice upon L. major infection. Hence, they expressed slower upregulation of keratinocyte markers implicated in the inhibition of wound healing, such as keratin 6a (Krt6a) and Krt16. This coincides with the presence of neutrophils displaying an altered phenotype characterized by a lower expression of surface markers Ly6C, CD11b, and Ly6G. These neutrophils exhibited very lower levels of apoptosis similarly to neutrophils present in resistant STAT6<sup>−/−</sup> mice. Interestingly, the reduced footpad swelling in DKO mice is associated with a high footpad parasite level similar to susceptible IL-12p40<sup>−/−</sup> mice. In conclusion, this study demonstrate that in the absence of both STAT6 and IL-12p40 signaling, L. major-infected mice display smaller and less ulcerated lesions, which does, however, not correlate with reduced parasite load. In addition, the presence of neutrophils with an altered phenotype is associated with reduced apoptosis and delayed immunopathologies, demonstrating the detrimental role of STAT6 in infected susceptible BALB/c mice.</p

    image_2.tiff

    No full text
    <p>Leishmania major (L. major) parasites are intracellular parasites belong to the Trypanosomatidae family and are the causative agent of cutaneous leishmaniasis. This disease affects approximately 1.5 million per year worldwide and there is currently no prophylactic vaccine available. L. major is transmitted by the bite of an infected sandfly and has been considered for decades now as a mouse model of choice to identify the factors implicated in T helper (Th)1 and Th2 polarization due to the natural resistance and susceptibility to infection of C57BL/6 and BALB/c mice, respectively. In this study, we refine the role of IL-12p40 cytokine, which is implicated the development of a protective Th1 response, and STAT6, a transcription factor involved in the signaling via detrimental interleukin (IL)-4 and IL-13 associated Th2 cytokines during L. major infection in the BALB/c model. In the absence of STAT6 and IL-12p40 signaling, double knockout (DKO) susceptible BALB/c mice displayed reduced footpad swelling and ulcerative lesion compared to IL-12p40<sup>−/−</sup> mice upon L. major infection. Hence, they expressed slower upregulation of keratinocyte markers implicated in the inhibition of wound healing, such as keratin 6a (Krt6a) and Krt16. This coincides with the presence of neutrophils displaying an altered phenotype characterized by a lower expression of surface markers Ly6C, CD11b, and Ly6G. These neutrophils exhibited very lower levels of apoptosis similarly to neutrophils present in resistant STAT6<sup>−/−</sup> mice. Interestingly, the reduced footpad swelling in DKO mice is associated with a high footpad parasite level similar to susceptible IL-12p40<sup>−/−</sup> mice. In conclusion, this study demonstrate that in the absence of both STAT6 and IL-12p40 signaling, L. major-infected mice display smaller and less ulcerated lesions, which does, however, not correlate with reduced parasite load. In addition, the presence of neutrophils with an altered phenotype is associated with reduced apoptosis and delayed immunopathologies, demonstrating the detrimental role of STAT6 in infected susceptible BALB/c mice.</p

    image_1.tif

    No full text
    <p>Leishmania major (L. major) parasites are intracellular parasites belong to the Trypanosomatidae family and are the causative agent of cutaneous leishmaniasis. This disease affects approximately 1.5 million per year worldwide and there is currently no prophylactic vaccine available. L. major is transmitted by the bite of an infected sandfly and has been considered for decades now as a mouse model of choice to identify the factors implicated in T helper (Th)1 and Th2 polarization due to the natural resistance and susceptibility to infection of C57BL/6 and BALB/c mice, respectively. In this study, we refine the role of IL-12p40 cytokine, which is implicated the development of a protective Th1 response, and STAT6, a transcription factor involved in the signaling via detrimental interleukin (IL)-4 and IL-13 associated Th2 cytokines during L. major infection in the BALB/c model. In the absence of STAT6 and IL-12p40 signaling, double knockout (DKO) susceptible BALB/c mice displayed reduced footpad swelling and ulcerative lesion compared to IL-12p40<sup>−/−</sup> mice upon L. major infection. Hence, they expressed slower upregulation of keratinocyte markers implicated in the inhibition of wound healing, such as keratin 6a (Krt6a) and Krt16. This coincides with the presence of neutrophils displaying an altered phenotype characterized by a lower expression of surface markers Ly6C, CD11b, and Ly6G. These neutrophils exhibited very lower levels of apoptosis similarly to neutrophils present in resistant STAT6<sup>−/−</sup> mice. Interestingly, the reduced footpad swelling in DKO mice is associated with a high footpad parasite level similar to susceptible IL-12p40<sup>−/−</sup> mice. In conclusion, this study demonstrate that in the absence of both STAT6 and IL-12p40 signaling, L. major-infected mice display smaller and less ulcerated lesions, which does, however, not correlate with reduced parasite load. In addition, the presence of neutrophils with an altered phenotype is associated with reduced apoptosis and delayed immunopathologies, demonstrating the detrimental role of STAT6 in infected susceptible BALB/c mice.</p

    image_4.tif

    No full text
    <p>Leishmania major (L. major) parasites are intracellular parasites belong to the Trypanosomatidae family and are the causative agent of cutaneous leishmaniasis. This disease affects approximately 1.5 million per year worldwide and there is currently no prophylactic vaccine available. L. major is transmitted by the bite of an infected sandfly and has been considered for decades now as a mouse model of choice to identify the factors implicated in T helper (Th)1 and Th2 polarization due to the natural resistance and susceptibility to infection of C57BL/6 and BALB/c mice, respectively. In this study, we refine the role of IL-12p40 cytokine, which is implicated the development of a protective Th1 response, and STAT6, a transcription factor involved in the signaling via detrimental interleukin (IL)-4 and IL-13 associated Th2 cytokines during L. major infection in the BALB/c model. In the absence of STAT6 and IL-12p40 signaling, double knockout (DKO) susceptible BALB/c mice displayed reduced footpad swelling and ulcerative lesion compared to IL-12p40<sup>−/−</sup> mice upon L. major infection. Hence, they expressed slower upregulation of keratinocyte markers implicated in the inhibition of wound healing, such as keratin 6a (Krt6a) and Krt16. This coincides with the presence of neutrophils displaying an altered phenotype characterized by a lower expression of surface markers Ly6C, CD11b, and Ly6G. These neutrophils exhibited very lower levels of apoptosis similarly to neutrophils present in resistant STAT6<sup>−/−</sup> mice. Interestingly, the reduced footpad swelling in DKO mice is associated with a high footpad parasite level similar to susceptible IL-12p40<sup>−/−</sup> mice. In conclusion, this study demonstrate that in the absence of both STAT6 and IL-12p40 signaling, L. major-infected mice display smaller and less ulcerated lesions, which does, however, not correlate with reduced parasite load. In addition, the presence of neutrophils with an altered phenotype is associated with reduced apoptosis and delayed immunopathologies, demonstrating the detrimental role of STAT6 in infected susceptible BALB/c mice.</p
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