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Role of Dectin-1 in the innate immune response of rat corneal epithelial cells to Aspergillus fumigatus.

Xu Q, Zhao G, Lin J, Wang Q, Hu L, Jiang Z - BMC Ophthalmol (2015)

Bottom Line: After 8 h of fungal stimulations, IL-6 and CXCL1 of pretreatment groups were still significantly (p < 0.05) lower than fungal groups.With progress of fungus stimulation, expression of IL-1β,CXCL1 ,CXCL2,MCP-1 gradually increased, whilepretreated with Laminarin to block Dectin-1, these expression decreased, indicating that Dectin-1 maypromote immune reaction through them.IL-10 decreased in fungal group because of itsimmunosuppressive effect at 4h, and it began to increase at 8h to suppress Th1 inflammation response inorder to avoid excessive tissue damage.

View Article: PubMed Central - PubMed

Affiliation: Affiliated Hospital of Qingdao University, 16th Jiangsu Road, Qingdao, Shandong Province, China. yankexuqiang@126.com.

ABSTRACT

Background: To observe Dectin-1 expression in fungal keratitis on rat models and to determine the role of Dectin-1 in innate immune response to Aspergillus fumigatus.

Methods: Wistar rats were randomly divided into control, fungal keratitis and pretreatment (pretreated with Laminarin) groups. Samples were used for conducting immunohistochemical staining and real-time PCR to observe expression of cytokines like CCL2, CCL3, CXCL1, CXCL2, IL-1β, TNF-α, IL-6, IL-10.

Results: After fungal stimulations, all 7 inflammatory factors, except IL-10, increased with different levels. After 4 h of fungal stimulations, IL-1β, IL-6, CCL2, CXCL1 and CXCL2 of pretreatment groups were significantly (p < 0.05) lower than fungal groups, while the other 3 cytokines had no significant changes. After 8 h of fungal stimulations, IL-6 and CXCL1 of pretreatment groups were still significantly (p < 0.05) lower than fungal groups.

Discussion: With progress of fungus stimulation, expression of IL-1β,CXCL1 ,CXCL2,MCP-1 gradually increased, whilepretreated with Laminarin to block Dectin-1, these expression decreased, indicating that Dectin-1 maypromote immune reaction through them. IL-10 decreased in fungal group because of itsimmunosuppressive effect at 4h, and it began to increase at 8h to suppress Th1 inflammation response inorder to avoid excessive tissue damage.

Conclusion: Dectin-1 in early period of innate immune responses in rat fungal keratitis might work through IL-1β, IL-6, CCL2, CXCL1, CXCL2 to recruit neutrophils and macrophages to participate anti-fungal immunity.

No MeSH data available.


Related in: MedlinePlus

Real-time RT-PCR results. After fungal stimulations, all 7 inflammatory factors, except IL-10, increased with different degrees, during which, IL-1β, TNF-α, CCL3 peaked at 16 h and decreased at 24 h, CXCL1 peaked at 4 h, IL-6 peaked at 8 h, CCL2 and CXCL2 continued rising. IL-10 decreased at 4 h, increased from 8 h, peaked at 16 h, and reduced from 24 h
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Fig3: Real-time RT-PCR results. After fungal stimulations, all 7 inflammatory factors, except IL-10, increased with different degrees, during which, IL-1β, TNF-α, CCL3 peaked at 16 h and decreased at 24 h, CXCL1 peaked at 4 h, IL-6 peaked at 8 h, CCL2 and CXCL2 continued rising. IL-10 decreased at 4 h, increased from 8 h, peaked at 16 h, and reduced from 24 h

Mentions: As shown in Figs. 3 and 4, expression of eight inflammatory factors mRNA was detected in every blank (normal rat) group. After 4 h of fungus stimulation, expression of IL-1β, IL-6, CCL2, CXCL1, CXCL2 increased and had significant difference (p < 0.05). After 8 h of fungus stimulation, expression of TNF-α and CCL3 increased more and had significant difference (p < 0.05). Expression of IL-10 was lower in 4 h fungus groups than control groups, and at 8 h fungus groups it increased and was statistically significant compared with control groups (p < 0.05). IL-1β, TNF-α and CCL3 reached maximum at 16 h, and then decreased from 24 h. CXCL1 increased from 4 h to 16 h, and then decreased. IL-6 reached peak at 8 h, then gradually decreased, while expression of CCL2 and CXCL2 continued to increase for all the time.Fig. 3


Role of Dectin-1 in the innate immune response of rat corneal epithelial cells to Aspergillus fumigatus.

Xu Q, Zhao G, Lin J, Wang Q, Hu L, Jiang Z - BMC Ophthalmol (2015)

Real-time RT-PCR results. After fungal stimulations, all 7 inflammatory factors, except IL-10, increased with different degrees, during which, IL-1β, TNF-α, CCL3 peaked at 16 h and decreased at 24 h, CXCL1 peaked at 4 h, IL-6 peaked at 8 h, CCL2 and CXCL2 continued rising. IL-10 decreased at 4 h, increased from 8 h, peaked at 16 h, and reduced from 24 h
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4591637&req=5

Fig3: Real-time RT-PCR results. After fungal stimulations, all 7 inflammatory factors, except IL-10, increased with different degrees, during which, IL-1β, TNF-α, CCL3 peaked at 16 h and decreased at 24 h, CXCL1 peaked at 4 h, IL-6 peaked at 8 h, CCL2 and CXCL2 continued rising. IL-10 decreased at 4 h, increased from 8 h, peaked at 16 h, and reduced from 24 h
Mentions: As shown in Figs. 3 and 4, expression of eight inflammatory factors mRNA was detected in every blank (normal rat) group. After 4 h of fungus stimulation, expression of IL-1β, IL-6, CCL2, CXCL1, CXCL2 increased and had significant difference (p < 0.05). After 8 h of fungus stimulation, expression of TNF-α and CCL3 increased more and had significant difference (p < 0.05). Expression of IL-10 was lower in 4 h fungus groups than control groups, and at 8 h fungus groups it increased and was statistically significant compared with control groups (p < 0.05). IL-1β, TNF-α and CCL3 reached maximum at 16 h, and then decreased from 24 h. CXCL1 increased from 4 h to 16 h, and then decreased. IL-6 reached peak at 8 h, then gradually decreased, while expression of CCL2 and CXCL2 continued to increase for all the time.Fig. 3

Bottom Line: After 8 h of fungal stimulations, IL-6 and CXCL1 of pretreatment groups were still significantly (p < 0.05) lower than fungal groups.With progress of fungus stimulation, expression of IL-1β,CXCL1 ,CXCL2,MCP-1 gradually increased, whilepretreated with Laminarin to block Dectin-1, these expression decreased, indicating that Dectin-1 maypromote immune reaction through them.IL-10 decreased in fungal group because of itsimmunosuppressive effect at 4h, and it began to increase at 8h to suppress Th1 inflammation response inorder to avoid excessive tissue damage.

View Article: PubMed Central - PubMed

Affiliation: Affiliated Hospital of Qingdao University, 16th Jiangsu Road, Qingdao, Shandong Province, China. yankexuqiang@126.com.

ABSTRACT

Background: To observe Dectin-1 expression in fungal keratitis on rat models and to determine the role of Dectin-1 in innate immune response to Aspergillus fumigatus.

Methods: Wistar rats were randomly divided into control, fungal keratitis and pretreatment (pretreated with Laminarin) groups. Samples were used for conducting immunohistochemical staining and real-time PCR to observe expression of cytokines like CCL2, CCL3, CXCL1, CXCL2, IL-1β, TNF-α, IL-6, IL-10.

Results: After fungal stimulations, all 7 inflammatory factors, except IL-10, increased with different levels. After 4 h of fungal stimulations, IL-1β, IL-6, CCL2, CXCL1 and CXCL2 of pretreatment groups were significantly (p < 0.05) lower than fungal groups, while the other 3 cytokines had no significant changes. After 8 h of fungal stimulations, IL-6 and CXCL1 of pretreatment groups were still significantly (p < 0.05) lower than fungal groups.

Discussion: With progress of fungus stimulation, expression of IL-1β,CXCL1 ,CXCL2,MCP-1 gradually increased, whilepretreated with Laminarin to block Dectin-1, these expression decreased, indicating that Dectin-1 maypromote immune reaction through them. IL-10 decreased in fungal group because of itsimmunosuppressive effect at 4h, and it began to increase at 8h to suppress Th1 inflammation response inorder to avoid excessive tissue damage.

Conclusion: Dectin-1 in early period of innate immune responses in rat fungal keratitis might work through IL-1β, IL-6, CCL2, CXCL1, CXCL2 to recruit neutrophils and macrophages to participate anti-fungal immunity.

No MeSH data available.


Related in: MedlinePlus