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Cryptocaryon irritans infection induces the acute phase response in Lates calcarifer: a transcriptomic perspective

Khoo CK, Abdul-Murad AM, Kua BC, Mohd-Adnan A

Fish Shellfish Immunol, 2012 Oct;33(4):788-94.
PMID: 22842150 DOI: 10.1016/j.fsi.2012.07.005

Cryptocaryoniasis (also known as marine white spot disease) is mediated by Cryptocaryon irritans. This obligate ectoparasitic protozoan infects virtually all marine teleosts, which includes Lates calcarifer, a highly valuable aquaculture species. Little is known about L. calcarifer-C. irritans interactions. This study was undertaken to gain an informative snapshot of the L. calcarifer transcriptomic response over the course of C. irritans infection. An in-house fabricated cDNA microarray slides containing 3872 probes from L. calcarifer liver and spleen cDNA libraries were used as a tool to investigate the response of L. calcarifer to C. irritans infection. Juvenile fish were infected with parasites for four days, and total RNA was extracted from liver tissue, which was harvested daily. We compared the transcriptomes of C. irritans-infected liver to uninfected liver over an infection period of four days; the comparison was used to identify the genes with altered expression levels in response to C. irritans infection. The greatest number of infection-modulated genes was recorded at 2 and 3 days post-infection. These genes were mainly associated with the immune response and were associated in particular with the acute phase response. Acute phase proteins such as hepcidin, C-type lectin and serum amyloid A are among the highly modulated genes. Our results indicate that an induced acute phase response in L. calcarifer toward C. irritans infection is similar to the responses observed in bacterial infections of teleosts. This response demonstrates the importance of first line defenses in teleost innate immune responses against ectoparasite infection.

Matched MeSH terms: Acute-Phase Reaction/etiology; Acute-Phase Reaction/parasitology
Fulltext Genome wide transcriptome profiling of a murine acute melioidosis model reveals new insights into how Burkholderia pseudomallei overcomes host innate immunity

Chin CY, Monack DM, Nathan S

BMC Genomics, 2010;11:672.
PMID: 21110886 DOI: 10.1186/1471-2164-11-672

At present, very little is known about how Burkholderia pseudomallei (B. pseudomallei) interacts with its host to elicit melioidosis symptoms. We established a murine acute-phase melioidosis model and used DNA microarray technology to investigate the global host/pathogen interaction. We compared the transcriptome of infected liver and spleen with uninfected tissues over an infection period of 42 hr to identify genes whose expression is altered in response to an acute infection.

Matched MeSH terms: Acute-Phase Reaction/complications; Acute-Phase Reaction/genetics; Acute-Phase Reaction/immunology
Fulltext Influence of Corynebacterium pseudotuberculosis infection on level of acute phase proteins in goats

Jeber ZK, MohdJin Z, Jesse FF, Saharee AA, Sabri J, Yusoff R, et al.

BMC Vet Res, 2016;12:48.
PMID: 26961495 DOI: 10.1186/s12917-016-0675-y

Goat caseous lymphadenitis (CLA) is a chronic disease caused by Corynebacterium pseudotuberculosis. However, there is paucity of data about goat's acute phase response during the course of CLA. This study was conducted to investigate the response of acute phase proteins, mainly haptoglobin (Hp), serum amyloid A (SAA) and the negative acute phase response, especially albumin after an experimental challenge of C. pseudotuberculosis and phospholipase D (PLD) in Cross bred Boer goats.

Matched MeSH terms: Acute-Phase Reaction
Ethnic differences in correlates of microalbuminuria in NIDDM. The role of the acute-phase response

Islam N, Kazmi F, Chusney GD, Mattock MB, Zaini A, Pickup JC

Diabetes Care, 1998 Mar;21(3):385-8.
PMID: 9540020

OBJECTIVE: To investigate whether microalbuminuria is associated with markers of the acute-phase response in NIDDM and whether there are ethnic differences in this association among the three main racial groups in Malaysia.
RESEARCH DESIGN AND METHODS: NIDDM patients of Chinese, Indian, and Malay origin attending a diabetic clinic in Kuala Lumpur, Malaysia, were matched for age, sex, diabetes duration, and glycemic control (n = 34 in each group). Urinary albumin-to-creatinine ratio was measured in an early morning urine sample. Biochemical measurements included markers of the acute-phase response: serum sialic acid, triglyceride, and (lowered) HDL cholesterol.
RESULTS: The frequency of microalbuminuria did not differ among the Chinese, Indian, and Malay patients (44, 41, and 47%, respectively). In Chinese patients, those with microalbuminuria had evidence of an augmented acute-phase response, with higher serum sialic acid and triglyceride and lower HDL cholesterol levels; and urinary albumin-to-creatinine ratio was correlated with serum sialic acid and triglyceride. The acute-phase response markers were not different in Indians, with microalbuminuria being high in even the normoalbuminuric Indians; only the mean arterial blood pressure was correlated with urinary albumin-to-creatinine ratio in the Indians. Malay NIDDM subjects had an association of microalbuminuria with acute-phase markers, but this was weaker than in the Chinese subjects.
CONCLUSIONS: Microalbuminuria is associated with an acute-phase response in Chinese NIDDM patients in Malaysia, as previously found in Caucasian NIDDM subjects. Elevated urinary albumin excretion has different correlates in other racial groups, such as those originating from the Indian subcontinent. The acute-phase response may have an etiological role in microalbuminuria.

Matched MeSH terms: Acute-Phase Reaction/blood; Acute-Phase Reaction/physiopathology; Acute-Phase Reaction/urine
Fulltext Concentration of serum amyloid a in clinically normal endurance horses in Malaysia

Rajendren, S.K., Khairuddin, N.H., Sumita, S.

Jurnal Veterinar Malaysia, 2019;31(1):28-33.
MyJurnal

Endurance horses continuously undergoing training. This will cause inflammation which leads to acute phase reaction with the production of acute phase protein, especially serum amyloid A (SAA). The purpose of this study was to establish concentration of SAA in normal endurance horses in the blood serum using two-site enzyme linked immunoassay (ELISA) technique. Horse sera were aliquoted from blood taken from jugular venipuncture. The highest concentration of SAA was observed in horses rested between 12 months and 24 months. The lowest concentration of SAA was noticed in horses rested more than 24 months. All the horses between 6 and 11 years old have high SAA concentration. When resting intervals were compared against gender of the horses, it was noted that all mares have high SAA concentration compared to gelding and stallion. Whereas SAA concentration in Thoroughbred horses were high compared to Arabian horses in all rest intervals. The SAA concentration in horses rested more than 24 months was low most probably because the horses recovered well from the inflammatory process happened during the endurance race.

Matched MeSH terms: Acute-Phase Reaction
Expression profile of immune-related genes in Lates calcarifer infected by Cryptocaryon irritans

Mohd-Shaharuddin N, Mohd-Adnan A, Kua BC, Nathan S

Fish Shellfish Immunol, 2013 Mar;34(3):762-9.
PMID: 23296118 DOI: 10.1016/j.fsi.2012.11.052

Cryptocaryon irritans causes Cyptocaryonosis or white spot disease in a wide range of marine fish including Lates calcarifer (Asian seabass). However, the immune response of this fish to the parasite is still poorly understood. In this study, quantitative polymerase chain reaction (qPCR) was performed to assess the expression profile of immune-related genes in L. calcarifer infected by C. irritans. A total of 21 immune-related genes encoding various functions in the fish immune system were utilized for the qPCR analysis. The experiment was initiated with the infection of juvenile fish by exposure to theronts from 200 C. irritans cysts, and non-infected juvenile fish were used as controls. Spleen, liver, gills and kidney tissues were harvested at three days post-infection from control and infected fish. In addition, organs were also harvested on day-10 post-infection from fish that had been allowed to recover from day-4 up to day-10 post-infection. L. calcarifer exhibited pathological changes on day-3 post-infection with the characteristic presence of white spots on the entire fish body, excessive mucus production and formation of a flap over the fish eye. High quality total RNA was extracted from all tissues and qPCR was performed. The qPCR analysis on the cohort of 21 immune-related genes of the various organs harvested on day-3 post-infection demonstrated that most genes were induced significantly (p

Matched MeSH terms: Acute-Phase Reaction/etiology; Acute-Phase Reaction/parasitology
Interleukin-6 inhibition of peroxisome proliferator-activated receptor alpha expression is mediated by JAK2- and PI3K-induced STAT1/3 in HepG2 hepatocyte cells

Chew GS, Myers S, Shu-Chien AC, Muhammad TS

Mol Cell Biochem, 2014 Mar;388(1-2):25-37.
PMID: 24242046 DOI: 10.1007/s11010-013-1896-z

Interleukin-6 (IL-6) is the major activator of the acute phase response (APR). One important regulator of IL-6-activated APR is peroxisome proliferator-activated receptor alpha (PPARα). Currently, there is a growing interest in determining the role of PPARα in regulating APR; however, studies on the molecular mechanisms and signaling pathways implicated in mediating the effects of IL-6 on the expression of PPARα are limited. We previously revealed that IL-6 inhibits PPARα gene expression through CAAT/enhancer-binding protein transcription factors in hepatocytes. In this study, we determined that STAT1/3 was the direct downstream molecules that mediated the Janus kinase 2 (JAK2) and phosphatidylinositol-3 kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathways in IL-6-induced repression of PPARα. Treatment of cells with pharmacological inhibitors of JAK2, PI3K, AKT, and mTOR attenuated the inhibitory effect of IL-6 on PPARα protein in a dose-dependent manner. These inhibitors also decreased the IL-6-induced repression of PPARα mRNA expression and promoter activity. Overexpression of STAT1 and STAT3 in HepG2 cells cotransfected with a reporter vector containing this PPARα promoter region revealed that both the expression plasmids inhibited the IL-6-induced repression of PPARα promoter activity. In the presence of inhibitors of JAK2 and mTOR (AG490 and rapamycin, respectively), IL-6-regulated protein expression and DNA binding of STAT1 and STAT3 were either completely or partially inhibited simultaneously, and the IL-6-induced repression of PPARα protein and mRNA was also inhibited. This study has unraveled novel pathways by which IL-6 inhibits PPARα gene transcription, involving the modulation of JAK2/STAT1-3 and PI3K/AKT/mTOR by inducing the binding of STAT1 and STAT3 to STAT-binding sites on the PPARα promoter. Together, these findings represent a new model of IL-6-induced suppression of PPARα expression by inducing STAT1 and STAT3 phosphorylation and subsequent down-regulation of PPARα mRNA expression.

Matched MeSH terms: Acute-Phase Reaction/genetics
Supplementation with tocotrienol-rich fraction alters the plasma levels of Apolipoprotein A-I precursor, Apolipoprotein E precursor, and C-reactive protein precursor from young and old individuals

Heng EC, Karsani SA, Abdul Rahman M, Abdul Hamid NA, Hamid Z, Wan Ngah WZ

Eur J Nutr, 2013 Oct;52(7):1811-20.
PMID: 23287846 DOI: 10.1007/s00394-012-0485-3

PURPOSE: Tocotrienol possess beneficial effects not exhibited by tocopherol. In vitro studies using animal models have suggested that these effects are caused via modulation of gene and protein expression. However, human supplementation studies using tocotrienol-rich isomers are limited. This study aims to identify plasma proteins that changed in expression following tocotrienol-rich fraction (TRF) supplementation within two different age groups.
METHODS: Subjects were divided into two age groups-32 ± 2 (young) and 52 ± 2 (old) years old. Four subjects from each group were assigned with TRF (78% tocotrienol and 22% tocopherol, 150 mg/day) or placebo capsules for 6 months. Fasting plasma were obtained at 0, 3, and 6 months. Plasma tocopherol and tocotrienol levels were determined. Plasma proteome was resolved by 2DE, and differentially expressed proteins identified by MS. The expressions of three proteins were validated by Western blotting.
RESULTS: Six months of TRF supplementation significantly increased plasma levels of tocopherols and tocotrienols. Proteins identified as being differentially expressed were related to cholesterol homeostasis, acute-phase response, protease inhibitor, and immune response. The expressions of Apolipoprotein A-I precursor, Apolipoprotein E precursor, and C-reactive protein precursor were validated. The old groups showed more proteins changing in expression.
CONCLUSIONS: TRF appears to not only affect plasma levels of tocopherols and tocotrienols, but also the levels of plasma proteins. The identity of these proteins may provide insights into how TRF exerts its beneficial effects. They may also be potentially developed into biomarkers for the study of the effects and effectiveness of TRF supplementation.

Matched MeSH terms: Acute-Phase Reaction