Chronic intestinal parasite infection can induce both persistent immune activation and defective responsiveness of T cells. This study aimed to assess the number and function of T regulatory (Treg) cells in children with intestinal parasite infection. We have studied the peripheral blood from 93 children, 53 of them parasitized with protozoa, helminths, or both; the remainder were non parasitized, healthy controls. The number and function of CD4(+) CD25(high) and CD4(+) Foxp3(+) cells were similar in parasitized and control children. In contrast, there was a significant increase in the levels of CD3(+) CD69(+), CD4(+) CTLA-4(+), and CD8(+) CD28(-) T cells in helminth infected children. Moreover, some of these patients showed a diminished response to CD3/CD28 stimulation in comparison with the control children. Our data strongly suggest that whilst Treg cells are not affected by intestinal parasite infection, CD3(+) CD69(+), CD4(+) CTLA-4(+) and CD8(+) CD28(-) lymphocytes may play an important, but as yet undetermined role in the diminished immune competence observed in parasitized children.
To learn more about controlling renal interstitial hydrostatic pressure (RIHP), we assessed its response to renal medullary direct interstitial volume expansion (rmDIVE = 100 μL bolus infusion/30 sec). Three experimental series (S) were performed in hydropenic, anesthetized, right‐nephrectomized, acute left renal‐denervated and renal perfusion pressure‐controlled rats randomly assigned to groups in each S. S1: Rats without hormonal clamp were contrasted before and after rmDIVE induced via 0.9% saline solution bolus (SS group) or 2% albumin in SS bolus (2% ALB + SS group). Subcapsular ΔRIHP rose slowly, progressively and similarly in both groups by ~3 mmHg. S2: Rats under hormonal clamp were contrasted before and after sham rmDIVE (time CTR group) and real rmDIVE induced via either SS bolus (SS group) or SS bolus containing the subcutaneous tissue fibroblast relaxant dibutyryl‐cAMP (SS + db‐cAMP group). ΔRIHP showed time, group, and time*group interaction effects with a biphasic response (early: ~1 mmHg; late: ~4 mmHg) in the SS group that was absent in the SS + db‐cAMP group. S3: Two groups of rats (SS and SS + db‐cAMP) under hormonal clamp were contrasted as in S2, producing similar ΔRIHP results to those of S2 but showing a slow, progressive, and indistinct decrease in renal outer medullary blood flow in both groups. These results provide highly suggestive preliminary evidence that the renal interstitium is capable of contracting reactively in vivo in response to rmDIVE with SS and demonstrate that such a response is abolished when db‐cAMP is interstitially and concomitantly infused.
Our prior (EB08 Abs.738.4) cross sectional study suggested that bilateral chronic aortic baroreceptor denervation (AD) induces salt‐sensitive normotension in rats. To assess this in depth, mean arterial pressure (MAP) was measured intra‐arterially over time (3 times) in two groups of conscious Wistar rats. The first time (PreDen) was measured in caudal artery before random sham (SH, n = 7) or real AD (n = 10); the second one was measured in left femoral artery after 7 days on low sodium diet (PostDen LNaD = 0.04% Na) and the third time was measured in right femoral artery after 21 days on high sodium diet (PostDen HNaD = 8% Na). The effectiveness of AD was judged by Box‐Cox transformation of PHE(1) and SNP (2) slope [((( [3 ‐ (HR2‐HR1/ MAP2‐MAP1)] −0.4) ‐1) / ‐0.046)] obtained in conscious state. Salt Sensitivity = SS = (PostDen HNaD MAP ‐ PostDen LNaD MAP, mmHg). Delta of MAP (PostDen MAP ‐ PreDen MAP, mmHg) on both LNaD and HNaD were calculated too. &p = 0.05, *p <0.003 vs SH and + p < 0.01, # p < 0.009 vs LNaD.PreDen PostDen PostDen SS Delta MAP DeltaMAPLNaD HNaD LNaD HNaDSH 105.0 114.0 122.0+ 7.7 9.0 16.7+±2.7 ±1.8 ±1.7 ±2.5 ±2.6 ±2.3AD 101.0 123.2& 134.5*# 11.3 22.2* 33.5*#±2.0 ±2.4 ±2.8 ±2.6 ±2.0 ±2.4ConclusionsWistar rats show salt‐sensitive normotension that chronic AD switches to salt‐sensitive hypertension. Supported by: CONACYT 62282
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