myd88 flox mice  (Jackson Laboratory)

Journal: Transboundary and Emerging Diseases

Article Title: Trichinella spiralis HSP70 Mediates Mice Immune Responses via TLR2/MyD88/ERK Signaling Pathway

doi: 10.1155/tbed/5533482

Figure Lengend Snippet: Recombinant Ts‐HSP70 promotes the expression of TLR2 and MyD88. Mouse macrophages were stimulated with 5, 10, 20, or 40 μg/mL rTs‐HSP70 for 12 h. Following stimulation, total cellular RNA and protein were extracted and analyzed. A. The effect of rTs‐HSP70 on the transcription level of TLR2 and MyD88 in mouse macrophage cells. B. Western blot analysis of the TLR2 and MyD88 expression in mouse macrophage cells after rTs‐HSP70 stimulation. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above the bars denote statistically significant differences ( p < 0.05), while the same letters indicate no significant difference.

Article Snippet: To verify whether rTs‐HSP70 activates the NF‐κB and MAPK pathways via the TLR2/MyD88 signaling pathway, we pretreated cells with a TLR2‐specific antibody (Novus Biologicals, Centennial, CO, USA) and the MyD88 inhibitor T6167923 (MedChemExpress, Monmouth Junction, NJ, USA).

Techniques: Recombinant, Expressing, Western Blot

Journal: Transboundary and Emerging Diseases

Article Title: Trichinella spiralis HSP70 Mediates Mice Immune Responses via TLR2/MyD88/ERK Signaling Pathway

doi: 10.1155/tbed/5533482

Figure Lengend Snippet: Recombinant Ts‐HSP70 affects mouse macrophage immune function via the TLR2/MyD88/ERK signaling pathway. Mouse macrophages were pretreated with a TLR2‐specific antibody (or control IgG) for 1 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min) and harvested for Western blot. In the MyD88 inhibition assay, RAW264.7 cells were pretreated with the MyD88 inhibitor T6167923 (5, 10 μg/mL; DMSO control) for 18 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min), and harvested for Western blot analysis. A. TLR2 blocking assay. B. MyD88 inhibition assay. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above bars indicate significant differences ( p < 0.05); the same letter indicates no significant difference.

Article Snippet: To verify whether rTs‐HSP70 activates the NF‐κB and MAPK pathways via the TLR2/MyD88 signaling pathway, we pretreated cells with a TLR2‐specific antibody (Novus Biologicals, Centennial, CO, USA) and the MyD88 inhibitor T6167923 (MedChemExpress, Monmouth Junction, NJ, USA).

Techniques: Recombinant, Control, Western Blot, Inhibition, Blocking Assay

Journal: Frontiers in Immunology

Article Title: Characterizing the impact of intracutaneous dissemination on host responses during Borrelia burgdorferi infection

doi: 10.3389/fimmu.2026.1850665

Figure Lengend Snippet: Dissemination of the oppA2tn mutant in immunocompromised mice. (A, B) Cartoon distribution of skin sites on the dorsum and ventrum of each mouse sampled during infection and percent of sites that cultured positive at 4 wpi for (A) C3H/MyD88 and (B) C3H/SCID mice. Tabulated results can be found in Supplementary Table 3 and skin sampling maps in Supplementary Figure 1B .

Article Snippet: Immunocompromised mouse studies used either C3H MyD88 -/- , a kind gift from Linda Bockenstedt (Yale University School of Medicine, New Haven, Connecticut, USA) or C3H SCID (C3SnSmn.Cg- Prkdc scid /J) mice (Jackson Laboratory).

Techniques: Mutagenesis, Infection, Cell Culture, Sampling

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet:

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Produced

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) NanoString-based analysis of Toll-like receptor ( Tlr ) and MyD88 expression in the brainstem of 45-day old control and Ndufs4 (-/-) mice (see Methods ). Black – Ndufs4 (Ctl), Red – Ndufs4 (-/-) (see Methods ). p-values reflect multiple testing corrected (Holm-Šídák method) pairwise t-tests. *p<0.05, ns and those not shown – not significant. B ) Taqman probe-based qPCR analysis of Tlr7, Tlr9 , and MyD88 expression in 50-day old control and Ndufs4 (-/-) mouse brainstem samples. Normalized to actin, included in each reaction. Black – Ndufs4 (Ctl), Red – Ndufs4 (-/-) (see Methods ). Relative expression calculated using relative standard curve approach. *p<0.05, ns – not significant, by Holm-Šídák method multiple-testing corrected pairwise t-tests with Welch’s correction (no assumption regarding standard deviation).

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Expressing, Control, Standard Deviation

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on overall weight trajectory in Nduf4 (-/-) mice (see Results, , ). Replicates (n’s) as indicated. B) Maximum weights of individual animals in A). Replicates (n’s) as indicated in A). ANOVA and pairwise comparisons were not statistically significant. C) Impact of enrofloxacin and MyD88 disruption on the onset of cachexia (weight loss) in Nduf4 (-/-) mice. No curves significantly different by pairwise log-rank comparison. Replicates (n’s) as indicated.

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Disruption, Comparison

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on ataxia onset in Nduf4 (-/-) mice. n’s as indicated. The dot (MyD88(-/-) cohort) represents an animal which died prior to presenting with ataxia. P-value shown indicates pairwise log-rank test comparisons between curves indicated - **p<0.005. B) Impact of enrofloxacin and MyD88 disruption on the onset of clasping in Nduf4 (-/-) mice. n’s as indicated. The dot (MyD88(-/-) cohort) represents an animal which died prior to presenting with clasping. P-value shown indicates pairwise log-rank test comparisons between curves indicated - **p<0.005.

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Disruption

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on survival in Nduf4 (-/-) mice (see Methods , introduction). P-values shown indicate pairwise log-rank test comparisons between curves indicated - **p=0.0087, *p<0.013. n’s as indicated. B) Cause of death in mice from A). FDIC – found dead in cage, cause of death unknown. C) Summary of findings. Enrofloxacin treatment modestly accelerates disease progression in the Ndufs4 (-/-) model, while loss of MyD88 modestly slows disease progression and extends survival.

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Disruption, Biomarker Discovery

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet:

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Produced

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) NanoString-based analysis of Toll-like receptor ( Tlr ) and MyD88 expression in the brainstem of 45-day old control and Ndufs4 (-/-) mice (see Methods ). Black – Ndufs4 (Ctl), Red – Ndufs4 (-/-) (see Methods ). p-values reflect multiple testing corrected (Holm-Šídák method) pairwise t-tests. *p<0.05, ns and those not shown – not significant. B ) Taqman probe-based qPCR analysis of Tlr7, Tlr9 , and MyD88 expression in 50-day old control and Ndufs4 (-/-) mouse brainstem samples. Normalized to actin, included in each reaction. Black – Ndufs4 (Ctl), Red – Ndufs4 (-/-) (see Methods ). Relative expression calculated using relative standard curve approach. *p<0.05, ns – not significant, by Holm-Šídák method multiple-testing corrected pairwise t-tests with Welch’s correction (no assumption regarding standard deviation).

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Expressing, Control, Standard Deviation

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on overall weight trajectory in Nduf4 (-/-) mice (see Results, , ). Replicates (n’s) as indicated. B) Maximum weights of individual animals in A). Replicates (n’s) as indicated in A). ANOVA and pairwise comparisons were not statistically significant. C) Impact of enrofloxacin and MyD88 disruption on the onset of cachexia (weight loss) in Nduf4 (-/-) mice. No curves significantly different by pairwise log-rank comparison. Replicates (n’s) as indicated.

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Disruption, Comparison

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on ataxia onset in Nduf4 (-/-) mice. n’s as indicated. The dot (MyD88(-/-) cohort) represents an animal which died prior to presenting with ataxia. P-value shown indicates pairwise log-rank test comparisons between curves indicated - **p<0.005. B) Impact of enrofloxacin and MyD88 disruption on the onset of clasping in Nduf4 (-/-) mice. n’s as indicated. The dot (MyD88(-/-) cohort) represents an animal which died prior to presenting with clasping. P-value shown indicates pairwise log-rank test comparisons between curves indicated - **p<0.005.

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Disruption

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on survival in Nduf4 (-/-) mice (see Methods , introduction). P-values shown indicate pairwise log-rank test comparisons between curves indicated - **p=0.0087, *p<0.013. n’s as indicated. B) Cause of death in mice from A). FDIC – found dead in cage, cause of death unknown. C) Summary of findings. Enrofloxacin treatment modestly accelerates disease progression in the Ndufs4 (-/-) model, while loss of MyD88 modestly slows disease progression and extends survival.

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Disruption, Biomarker Discovery

Journal: Physiological Reports

Article Title: Water intake regulates mucosal immunity in rat jejunal villi via IL ‐1β, IL ‐6, and IL ‐10

doi: 10.14814/phy2.70891

Figure Lengend Snippet: (a) Effects of water intake on changes in lymph volume collected over set intervals of 60 min in rat jejunum‐derived lymph vessels in the absence (white column) and presence of a MyD88 inhibitor (oblique line column). (b) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐1β in the lymph. (c) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐6 in the lymph. (d) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐10 in the lymph. The error bars represent the SDs.

Article Snippet: Clodronate‐containing liposomes (catalog no 16001004, Sigma‐Aldrich, USA) and an inhibitor of MyD88 (catalog no 2‐29328 Novus Bio, USA) are purchased.

Techniques: Derivative Assay, Concentration Assay