Lactobacillus acidophilus

A Microbial Biorealm page on the genus Lactobacillus acidophilus

Classification

Higher order taxa

Bacteria; Firmicutes; Bacilli; Lactobacillales; Lactobacillaceae; Lactobacillus

Species

L. acidophilus

NCBI: Taxonomy Genome

Strains

Laboratory: NCFM, 4962, CNRZ216, CNRZ218

Human: HA1, HA2, HA3, HM2, HM6

Pig: PA3, PA12, PA19, P18, P47

Chicken: C1, C2, C3, C7, C11

Description and Significance

In general, Lactobacilli inhabit the gastrointestinal (GI) tract of humans and animals. Lactobacilli are considered to have a probiotic effect that contributes to overall health and well being.

Of the Lactobacillus species, L. acidophilus is the most well known and is commercially distributed as a probiotic. Early studies of L. acidophilus were performed on strains isolated from fecal material of humans, pigs and chickens. It has been characterized as a short gram-positive rod (2-10μm), homofermentative and optimal growth temperatures of 37˚C-42˚C.[1]

Further isolation and investigation into the physiological, biochemical, genetic, and fermentative properties have been widely explored in both humans and animals. The L. acidophilus strain, NCFM, has been commercially available in the United States as a probiotic strain since the mid-1970s. [2]

Genome structure

The complete circular genome of the NCFM strain of L. acidophilus contains 1,993,564 nucleotides. The DNA GC content was determined to be 34.71%. There are 1,7864 ORFs and 72.5% have been classified functionally.[3]

L. acidophilus NCFM contains no plasmids. [4]

Cell structure and metabolism

L. acidophilus grows in low pH (<3.5), anaerobic conditions and undergoes fermentation only.[5]

In 1999, an H⁺ induced ATPase was identified in L. acidophilus. Based on primary structure and the genetic organization, it was further classified as a F₁F₀-type ATPase. Its similarity to the streptococcal ATPase and the H⁺ inducibility of the operon suggests that it is responsible for an ATP-dependent exclusion of protons in order to maintain cytoplasmic pH (~7).[http://www.blackwell-synergy.com/doi/full/10.1046/j.1365-2958.1999.01557.x

L. acidophilus lack cytochromes, porphyrins, and respiratory enzymes and are therefore unable to undergo any oxidative phosphorylation or respiration. Because they utilize sugars as their substrates for fermentation, they inhabit environments with high sugar abundance, such as the GI tract in humans and animals. More specifially, L. acidophilus is homofermentative which means that they only byproduct it forms from fermentation is lactic acid. For every one glucose molecule that undergoes fermentation in L. acidophilus, the energy yield is two ATPs. As a result, homofermentative microbes must catabolize large amounts of substrate to generate enough energy for growth. In addition to glucose, L. acidophilus utilizes aesculin, cellobiose, galactose, lactose, maltose, salicin, sucrose, and trehalose for fermentation.

Pathology

The exact mechanism of the probiotic effect is still under investigation.

Adherence and colonization is one of many suggested mechanisms responsible for the probiotic effect of L. acidophilus. Adherence and colonization of the intestinal epithelium can act in two ways: (1) competition for space in on the epithelium and (2) interaction with enterocytes. There is some evidence that L. acidophilus NCFM has the ability adhere through a protein mediated mechanism. (see Current Research) After L. acidophilus has colonized the GI tract, as a probiotic bacteria it has the potential to influence the existing microbial population. [6]

Antimicrobial activity is a considered an important mechanism by which probiotic bacteria act to inhibit a range of microbes that have potentially detrimental effects. It is suggested that L. acidophilus produces bacteriocins (proteins that are active against other bacteria). This specific mechanism is currently being researched (see Current Research).[7]

L. acidophilus has been suggested as a supplement for lactose intolerant individuals. When taken orally and in sufficient dosages, there is evidence for a decrease in symptoms of lactose maldigestion. Presumably, the L. acidophilus colonizes the GI tract and contributes to the metabolism of lactose during digestion and transit through the GI tract.[8]