Saccharomyces cerevisiae var. boulardii CNCM I-1079 and Lactobacillus acidophilus BT1386 influence innate immune response and serum levels of acute-phase proteins during weaning in Holstein calves

2018 ◽  
Vol 98 (3) ◽  
pp. 576-588 ◽  
Author(s):  
Bridget E. Fomenky ◽  
Johanne Chiquette ◽  
Martin Lessard ◽  
Nathalie Bissonnette ◽  
Guylaine Talbot ◽  
...  

The aims of this study were to investigate the effect of Saccharomyces cerevisiae var. boulardii CNCM I-1079 (SCB) or Lactobacillus acidophilus BT1386 (LA) on (1) innate immune response, (2) markers of acute-phase reaction, and (3) immune gene expression of rumen and ileum tissues of Holstein calves. Forty eight calves (∼5 d old) were randomly allocated to four treatments as follows: (1) control (CTRL) fed milk replacer followed by starter feed, (2) CTRL supplemented with SCB in milk and feed, (3) CTRL supplemented with LA in milk and feed, and (4) CTRL supplemented with antibiotics (ATB; chlortetracycline and neomycin in milk, and chlortetracycline in feed). Tumor necrosis factor α (TNF-α) decreased (P < 0.05) on day 66 (post-weaning) for the ATB-treated calves. There were no treatment effects on production of interferon γ (IFN-γ) and interleukin 6 (IL-6) proteins and on expression of TLR4, TLR6, TLR9, TLR10, CLDN3, MUC1, and MUC20 genes. Calves fed SCB or LA had a greater (P < 0.05) oxidative burst at weaning (day 53) compared with CTRL. Oxidative burst was also greater (P < 0.05) after weaning (day 59 and day 87) for SCB-fed calves. Calves fed SCB and ATB had higher (P < 0.05) phagocytosis activity during weaning (day 47) compared with CTRL. The concentration of serum amyloid A2 (SAA2) increased (P < 0.05) in SCB- and LA-fed calves (day 53), whereas the concentration of C-reactive protein (CRP) increased (P < 0.05) in SCB-fed calves during weaning as compared with CTRL. Our results suggest that SCB could improve innate immune response (oxidative burst and phagocytosis) and markers of acute-phase reaction (CRP and SAA2), especially during critical periods like weaning.

2013 ◽  
Vol 154 (32) ◽  
pp. 1247-1255 ◽  
Author(s):  
Lajos Jakab

The acute and chronic constitutional reactions of the organism elicited by sterile causes and pathogenic structures threatening the soundness of the organism are surveyed by the author. It is emphasized that depending on causes which can be very different, there are various syndromes occurring in the clinical practice. On the basis of multitudiness of pathogenic factors and individual differences, the infammatory reactions are clinically, pathologically and pathobiochemically can be hugely variable. The acute inflammatory response may be sterile. It is often difficult to recognize in these processes whether the inflammation is harmful or beneficial for the organism as a whole. It is possible that the inflammatory response itself is the defending resource of the individual. The non-sterile acute inflammation is evoked by pathogenic microorganisms. The variety of clinical syndromes are explained by the high diversity of pathogenic microbes, the individualities of the defending organisms, and the natural and adaptive immunity of the organism which may be intact or possibly defective. In the latter case the inflammation itself is the disease, as a consequence of a pathological process conducted by the cortico-hypothalamo-adernal axis. The acute inflammation is a defending, preventing and repairing process, constituting an important part of the natural innate immune response. It is inseparable from the natural innate immune response, which is in close cooperation with the adaptive, specific immune response with mutual effects on each of the other. The conductor and the response reactions of the two immune responses are also the same. There are alterations in serum proteins/glycoproteins synthesized mostly by the hepatocytes. Because the concentration of almost all proteins/glycoproteins may change, the use of the discriminative term “acute phase reactant” is hardly relevant. For example, the HDL molecule is a negative “acute phase reactant”. On the gound of clinical, pathological and biochemical caracteristics, the chronic sterile inflammation is a very different entity. It has been established that atherosclerosis is one of the ab origine chronic inflammatory syndrome. It is a long-lasting pathological entity progressing, rather than resolving with different celerity, namely a unique vasculitis syndrome. We are speaking about risk factors instead of causes, which constitute larger or smaller groups to elicite the preventing reaction of the host. The propagations and final outcomes are quite different from that of the acute process. The disadvantages or benefits for the organism are scarcely predictable, albeit the chronic process may have roles in its prolonged nature. Orv. Hetil., 2013, 154, 1247–1255.


2020 ◽  
Vol 11 ◽  
Author(s):  
Jacintha G. B. van Dijk ◽  
Josanne H. Verhagen ◽  
Arne Hegemann ◽  
Conny Tolf ◽  
Jenny Olofsson ◽  
...  

Domestic mallards (Anas platyrhynchos domesticus) are traditionally used as a model to investigate infection dynamics and immune responses to low pathogenic avian influenza viruses (LPAIVs) in free-living mallards. However, it is unclear whether the immune response of domestic birds reflects the response of their free-living counterparts naturally exposed to these viruses. We investigated the extent to which the innate humoral immune response was similar among (i) wild-type domestic mallards in primary and secondary infection with LPAIV H4N6 in a laboratory setting (laboratory mallards), (ii) wild-type domestic mallards naturally exposed to LPAIVs in a semi-natural setting (sentinel mallards), and (iii) free-living mallards naturally exposed to LPAIVs. We quantified innate humoral immune function by measuring non-specific natural antibodies (agglutination), complement activity (lysis), and the acute phase protein haptoglobin. We demonstrate that complement activity in the first 3 days after LPAIV exposure was higher in primary-exposed laboratory mallards than in sentinel and free-living mallards. LPAIV H4N6 likely activated the complement system and the acute phase response in primary-exposed laboratory mallards, as lysis was higher and haptoglobin lower at day 3 and 7 post-exposure compared to baseline immune function measured prior to exposure. There were no differences observed in natural antibody and haptoglobin concentrations among laboratory, sentinel, and free-living mallards in the first 3 days after LPAIV exposure. Our study demonstrates that, based on the three innate humoral immune parameters measured, domestic mallards seem an appropriate model to investigate innate immunology of their free-living counterparts, albeit the innate immune response of secondary-LPAIV exposed mallards is a better proxy for the innate immune response in pre-exposed free-living mallards than that of immunologically naïve mallards.


2007 ◽  
Vol 28 (3) ◽  
pp. 450-455 ◽  
Author(s):  
Fernanda Marques ◽  
Ana-João Rodrigues ◽  
João C Sousa ◽  
Giovanni Coppola ◽  
Daniel H Geschwind ◽  
...  

Lipocalin 2 (LCN2) is able to sequester iron-loaded bacterial siderophores and, therefore, is known to participate in the mammalian innate immune response. Of notice, LCN2 was shown to display bacteriostatic effects both in in vitro and in vivo. To reach the brain, bacteria must cross the blood—brain or the choroid plexus (CP)/cerebrospinal fluid (CSF) barriers. Additionally, as the CP is responsible for the production of most of the CSF, responses of the CP mediate signaling into the brain. We show here that in conditions of peripheral inflammation, LCN2 behaves as an acute phase protein in the CP. As early as 1 h after lipopolysaccharide peripheral administration, Lcn2 mRNA levels are upregulated, returning to basal levels after 72 h. Increased LCN2 protein is observed in choroidal epithelia and in endothelial cells of blood vessels in the brain parenchyma. Higher levels of LCN2 are also present in the CSF. These observations suggest that expression of LCN2 at the CP/CSF barrier might be bacteriostatic in the brain, avoiding bacteria dissemination within the CSF into the brain parenchyma. This study shows that the LCN2 is produced by the CP as a component of the innate immune response that protects the central nervous system from infection.


Sign in / Sign up

Export Citation Format

Share Document